channelrhodopsin-2

Retrograde labeling of Sp5C projection neurons was greater when injections were made in young adult animals.

A key milestone described by the review is partial vision restoration in a human patient using ChrimsonR with light-amplifying goggles.

Within Sp5C, rgAAV and AAV9 produced similar levels of projection-neuron labeling in superficial and deep regions.

Red-shifted opsins including ReaChR and ChrimsonR reduce phototoxicity by enabling activation under longer wavelengths.

For both serotypes, labeled Sp5C projection neurons were found bilaterally with a strong ipsilateral bias.

Cre-dependent recombination successfully enabled selective channelrhodopsin-2 expression in Sp5C projection neurons.

rgAAV and AAV9 produce strong Sp5C projection-neuron transduction and provide a basis for future study of Sp5C projection-neuron afferent and efferent functions.

Following unilateral PBN injections, both rgAAV and AAV9 retrogradely labeled many Sp5C projection neurons.

Chronos provides superior temporal kinetics for dynamic visual tracking.

MCO1 optimized opsin performance under ambient light, helping bridge optogenetic vision restoration toward real-world applications.

rgAAV and AAV9 were evaluated as viral serotypes for identifying and analyzing Sp5C projection neurons that project to the parabrachial nucleus.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

A combination of ElectroFluor 730p, X-Rhod-1, and ChR2 in mouse hearts enables simultaneous monitoring of transmembrane potential and cytosolic calcium while performing optogenetic manipulation with minimal crosstalk.

We here present a novel approach to simultaneously monitor transmembrane potential and cytosolic calcium, while also performing optogenetic manipulation. For this, we used the novel voltage-sensitive dye ElectroFluor 730p and the cytosolic calcium indicator X-Rhod-1 in mouse hearts expressing channelrhodopsin-2 (ChR2). By exploiting the isosbestic point of ElectroFluor 730p and avoiding the ChR2 activation spectrum, we here introduce a novel optical imaging and manipulation approach with minimal crosstalk.

Recent work has used green light-gated ion channels to control plant growth and cellular motion.

We summarize the recent results of work in the field to control plant growth and cellular motion via green light-gated ion channels

Recent work has used green light-gated ion channels to control plant growth and cellular motion.

We summarize the recent results of work in the field to control plant growth and cellular motion via green light-gated ion channels

Recent work has used green light-gated ion channels to control plant growth and cellular motion.

We summarize the recent results of work in the field to control plant growth and cellular motion via green light-gated ion channels

Recent work has used green light-gated ion channels to control plant growth and cellular motion.

We summarize the recent results of work in the field to control plant growth and cellular motion via green light-gated ion channels

Recent work has used green light-gated ion channels to control plant growth and cellular motion.

We summarize the recent results of work in the field to control plant growth and cellular motion via green light-gated ion channels

Recent work has used green light-gated ion channels to control plant growth and cellular motion.

We summarize the recent results of work in the field to control plant growth and cellular motion via green light-gated ion channels

Recent work has used green light-gated ion channels to control plant growth and cellular motion.

We summarize the recent results of work in the field to control plant growth and cellular motion via green light-gated ion channels

Single or combined photoswitches have been successfully applied for light-controlled gene expression in plants.

present successful applications to light-control gene expression with single or combined photoswitches in plants

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Channelrhodopsin-2 is described as enabling millisecond neuromodulation.

Since the first demonstration of the millisecond neuromodulation ability of the channelrhodopsin-2 (ChR2)

Optogenetic technology progressed rapidly in basic life science research, especially neurobiology, after the first demonstration of ChR2-based millisecond neuromodulation.

the application of optogenetic technology in basic life science research has been rapidly progressed, especially in neurobiology

Channelrhodopsin-2-based optogenetic approaches can offer low-energy and localized control.

ChR2 expression in retinal ganglion cells of blind mice served as an early feasibility demonstration for optogenetic vision restoration.

Our first demonstration of the feasibility of such an approach involved expressing ChR2 in the retinal ganglion cells of blind mice

Implantable optical devices are being extensively developed for studying cardiac electrophysiological phenomena with precise optogenetic control.

Translation of implantable optogenetic technology toward clinical cardiovascular applications remains difficult and requires potential solutions.

These reviewed tools serve as powerful technical means to explore mechanisms underlying disease models and to evaluate drug effects in neuroscience.

CLARITY technology and optogenetics can be used to visualize neuronal circuits in whole-brain samples.

Tracer-based magnetic resonance imaging can be used to visualize the interstitial system of the brain.

The review covers MALDI time-of-flight mass spectrometry imaging, tracer-based MRI, CLARITY technology, and optogenetics as CNS study tools.

Spectrally shifted opsin variants can support enhanced tissue penetration, combinatorial stimulation of different cell subpopulations, and all-optical read-in and read-out studies.

The paper includes biocompatibility characterization of the implant platform.

The paper reports chronic rat pacing for up to 6 days.

The paper reports ex vivo optogenetic pacing in ChR2 hearts.

In cardiac physiology, optogenetics has mainly used optically controlled depolarizing ion channels to control heart rate and for optogenetic defibrillation.

Cardiac optogenetic stimulation can be read out using patch clamp, multi-unit microarray recordings, Langendorff heart electrical recordings, and optical reporters including small detecting molecules or genetically encoded sensors.

Optogenetic techniques use genetically expressed light-gated microbial channels or pumps to modulate cellular excitability with millisecond precision.

Cochlear optogenetics and optical cochlear implant work are framed around improved spectral selectivity relative to electrical cochlear implants.

The anchor article ... sits in the cochlear optogenetics / optical cochlear implant literature centered on spiral ganglion neuron (SGN) stimulation for improved spectral selectivity over electrical cochlear implants.

ChR2-expressing cardiomyocytes show normal baseline and active excitable membrane and Ca2+ signaling properties and are sensitive even to approximately 1 ms light pulses.

Expression of the chosen optogenetic tool in cardiac cells requires gene introduction by viral transduction or coupling via spark cells at the single-cell level, and transgenic expression or in vivo adenoviral delivery at system level.

Light delivery by laser or LED is relatively straightforward in vitro but is challenged in cardiac tissue by motion and light scattering.

The review includes caged compounds, photoswitchable tethered ligands, and engineered light-sensitive receptors or channels as optical control modalities.

The review explicitly spans optogenetics and optopharmacology/photopharmacology for neuronal ion channels and neurotransmitter receptors, including caged compounds, photoswitchable tethered ligands, and engineered light-sensitive receptors/channels.

Biophysical properties of microbial opsins determine their ability to evoke reliable and precise stimulation or silencing of electrophysiological activity.

The implant platform includes wireless energy-harvesting and digital communication electronics for battery-free operation.

The implant platform supports both electrical and optical stimulation.

The paper presents wireless, battery-free, fully implantable multimodal and multisite pacemakers for applications in small animal models.

Named platforms aligned with the review's scope include LiGluR, LiGluN, LimGluR, optogating, ChR2, and Arch.

Primary papers for specific photoswitchable receptor platforms explicitly named in or strongly aligned with the review (LiGluR, LiGluN, LimGluR, optogating of P2X2)... Channelrhodopsin-2 (ChR2)... Arch.

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

The ChR2 C128T mutant has a markedly increased open-state lifetime.

the C128T mutant, which has a markedly increased open-state lifetime

The ChR2 C128T mutant has a markedly increased open-state lifetime.

the C128T mutant, which has a markedly increased open-state lifetime

The ChR2 C128T mutant has a markedly increased open-state lifetime.

the C128T mutant, which has a markedly increased open-state lifetime

The ChR2 C128T mutant has a markedly increased open-state lifetime.

the C128T mutant, which has a markedly increased open-state lifetime

The ChR2 C128T mutant has a markedly increased open-state lifetime.

the C128T mutant, which has a markedly increased open-state lifetime

The ChR2 C128T mutant has a markedly increased open-state lifetime.

the C128T mutant, which has a markedly increased open-state lifetime

The ChR2 C128T mutant has a markedly increased open-state lifetime.

the C128T mutant, which has a markedly increased open-state lifetime

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

Channelrhodopsin 2 is a major optogenetic tool.

The light-gated ion channel channelrhodopsin 2 (ChR2) from Chlamydomonas reinhardtii is a major optogenetic tool.

Channelrhodopsin 2 is a major optogenetic tool.

The light-gated ion channel channelrhodopsin 2 (ChR2) from Chlamydomonas reinhardtii is a major optogenetic tool.

Channelrhodopsin 2 is a major optogenetic tool.

The light-gated ion channel channelrhodopsin 2 (ChR2) from Chlamydomonas reinhardtii is a major optogenetic tool.

Channelrhodopsin 2 is a major optogenetic tool.

The light-gated ion channel channelrhodopsin 2 (ChR2) from Chlamydomonas reinhardtii is a major optogenetic tool.

Channelrhodopsin 2 is a major optogenetic tool.

The light-gated ion channel channelrhodopsin 2 (ChR2) from Chlamydomonas reinhardtii is a major optogenetic tool.

Channelrhodopsin 2 is a major optogenetic tool.

The light-gated ion channel channelrhodopsin 2 (ChR2) from Chlamydomonas reinhardtii is a major optogenetic tool.

Channelrhodopsin 2 is a major optogenetic tool.

The light-gated ion channel channelrhodopsin 2 (ChR2) from Chlamydomonas reinhardtii is a major optogenetic tool.

Optogenetic defibrillation using cardiac ChR2 expression effectively terminated ventricular arrhythmias in mouse hearts.

Combining channelrhodopsin-2 with halorhodopsin enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

The combination of ChR2 with hyperpolarizing-light-driven ion pumps such as the Cl(-) pump halorhodopsin (NpHR) enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

Combining channelrhodopsin-2 with halorhodopsin enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

The combination of ChR2 with hyperpolarizing-light-driven ion pumps such as the Cl(-) pump halorhodopsin (NpHR) enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

Combining channelrhodopsin-2 with halorhodopsin enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

The combination of ChR2 with hyperpolarizing-light-driven ion pumps such as the Cl(-) pump halorhodopsin (NpHR) enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

Combining channelrhodopsin-2 with halorhodopsin enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

The combination of ChR2 with hyperpolarizing-light-driven ion pumps such as the Cl(-) pump halorhodopsin (NpHR) enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

Combining channelrhodopsin-2 with halorhodopsin enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

The combination of ChR2 with hyperpolarizing-light-driven ion pumps such as the Cl(-) pump halorhodopsin (NpHR) enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

Combining channelrhodopsin-2 with halorhodopsin enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

The combination of ChR2 with hyperpolarizing-light-driven ion pumps such as the Cl(-) pump halorhodopsin (NpHR) enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

Combining channelrhodopsin-2 with halorhodopsin enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

The combination of ChR2 with hyperpolarizing-light-driven ion pumps such as the Cl(-) pump halorhodopsin (NpHR) enables multimodal remote control of neuronal cells in culture, tissue, and living animals.

New genetically encoded tools have been applied to feeding circuits that regulate appetite.

This chapter reviews the application of new genetically encoded tools in feeding circuits that regulate appetite.

Rapid activation and inhibition of AgRP neurons established a causal role for rapid control of food intake.

Rapid activation and inhibition of agouti related peptide (AgRP) neurons conclusively established a causal role for rapid control of food intake.

Chemogenetic activation of AgRP neurons using hM3Dq avoids the invasive protocols required for ChR2 activation.

Chemogenetic activation of AgRP neurons using hM3Dq avoids the invasive protocols required for ChR2 activation.

Optical VTA stimulation does not restore righting or produce EEG changes in control DAT-cre mice targeted with a viral vector lacking ChR2 during steady-state isoflurane anesthesia.

AAV-based gene transfer of ChR2 enabled effective optogenetic termination of ventricular arrhythmias in WT mouse hearts.

D1 receptor antagonist pretreatment inhibits the arousal and righting-restoration effects of optical stimulation of VTA dopamine neurons during isoflurane anesthesia.

Ventricular tachycardia termination was attributed to ChR2-mediated transmural depolarization that blocks voltage-dependent Na+ channels throughout the myocardial wall and interrupts wavefront propagation into illuminated tissue.

Channelrhodopsin-2 enables activation of electrically excitable cells through light-dependent depolarization.

The most prominent example is channelrhodopsin-2 (ChR2), which allows the activation of electrically excitable cells via light-dependent depolarization.

Channelrhodopsin-2 enables activation of electrically excitable cells through light-dependent depolarization.

The most prominent example is channelrhodopsin-2 (ChR2), which allows the activation of electrically excitable cells via light-dependent depolarization.

Channelrhodopsin-2 enables activation of electrically excitable cells through light-dependent depolarization.

The most prominent example is channelrhodopsin-2 (ChR2), which allows the activation of electrically excitable cells via light-dependent depolarization.

Channelrhodopsin-2 enables activation of electrically excitable cells through light-dependent depolarization.

The most prominent example is channelrhodopsin-2 (ChR2), which allows the activation of electrically excitable cells via light-dependent depolarization.

Channelrhodopsin-2 enables activation of electrically excitable cells through light-dependent depolarization.

The most prominent example is channelrhodopsin-2 (ChR2), which allows the activation of electrically excitable cells via light-dependent depolarization.

Channelrhodopsin-2 enables activation of electrically excitable cells through light-dependent depolarization.

The most prominent example is channelrhodopsin-2 (ChR2), which allows the activation of electrically excitable cells via light-dependent depolarization.

Channelrhodopsin-2 enables activation of electrically excitable cells through light-dependent depolarization.

The most prominent example is channelrhodopsin-2 (ChR2), which allows the activation of electrically excitable cells via light-dependent depolarization.

ChR2 distributes into axons, enabling selective optogenetic activation of AgRP neuron axon projection fields in distinct brain areas to examine their contribution to feeding behavior.

ChR2 distributes into axons, and selective optogenetic activation of AgRP neuron axon projection fields in distinct brain areas was used to examine their individual contribution to feeding behavior.

In diseased ChR2-expressing human heart simulations, red light effectively terminated ventricular tachycardia.

Selective optogenetic activation of VTA dopamine neurons is sufficient to induce arousal from an anesthetized unconscious state during steady-state isoflurane anesthesia.

GCaMP6s is used in the review context as an activity reporter example for zebrafish brain imaging.

The anchor figure caption explicitly cites GCaMP6s for zebrafish brain activity imaging.

LOVpep and ePDZ are presented in the review context as a light-induced intracellular trafficking control system.

The anchor figure caption names LOVpep and ePDZ in a light-induced trafficking example.

Optopatch is presented in the review context as an all-optical electrophysiology system with CheRiff and QuasAr2 as named components.

PubMed figure captions ... explicitly mention tool/component names used in the review, especially Optopatch/CheRiff/QuasAr2.

The review context includes inhibitory opsins, excitatory opsins, closed-loop seizure detection, and luminopsin-based approaches as relevant seizure-control tools or components.

Explicitly supported component/tool names found in these sources include NpHR, ChR2, ArchT, closed-loop real-time seizure detection, and inhibitory luminopsins.

pMag and nMag are presented in the review context as a light-induced dimerization pair used to reconstitute split Cas9 in photoactivatable genome editing.

The anchor figure caption names pMag as one half of the light-induced dimerization pair used to reconstitute split Cas9 ... nMag as the partner to pMag.

Optogenetic defibrillation could potentially be translated into humans to achieve nondamaging and pain-free termination of ventricular arrhythmia.

Optical modulation for optogenetic assays can be obtained in a miniaturized 384-well plate format using the FLIPR instrument.

we sought to determine if this optical modulation can be obtained also in a miniaturized format, such as a 384-well plate, using the instrumentations normally dedicated to fluorescence analysis in High Throughput Screening (HTS) activities, such as for example the FLIPR (Fluorometric Imaging Plate Reader) instrument

Optical modulation for optogenetic assays can be obtained in a miniaturized 384-well plate format using the FLIPR instrument.

we sought to determine if this optical modulation can be obtained also in a miniaturized format, such as a 384-well plate, using the instrumentations normally dedicated to fluorescence analysis in High Throughput Screening (HTS) activities, such as for example the FLIPR (Fluorometric Imaging Plate Reader) instrument

Optical modulation for optogenetic assays can be obtained in a miniaturized 384-well plate format using the FLIPR instrument.

we sought to determine if this optical modulation can be obtained also in a miniaturized format, such as a 384-well plate, using the instrumentations normally dedicated to fluorescence analysis in High Throughput Screening (HTS) activities, such as for example the FLIPR (Fluorometric Imaging Plate Reader) instrument

Optical modulation for optogenetic assays can be obtained in a miniaturized 384-well plate format using the FLIPR instrument.

we sought to determine if this optical modulation can be obtained also in a miniaturized format, such as a 384-well plate, using the instrumentations normally dedicated to fluorescence analysis in High Throughput Screening (HTS) activities, such as for example the FLIPR (Fluorometric Imaging Plate Reader) instrument

Optical modulation for optogenetic assays can be obtained in a miniaturized 384-well plate format using the FLIPR instrument.

we sought to determine if this optical modulation can be obtained also in a miniaturized format, such as a 384-well plate, using the instrumentations normally dedicated to fluorescence analysis in High Throughput Screening (HTS) activities, such as for example the FLIPR (Fluorometric Imaging Plate Reader) instrument

Optical modulation for optogenetic assays can be obtained in a miniaturized 384-well plate format using the FLIPR instrument.

we sought to determine if this optical modulation can be obtained also in a miniaturized format, such as a 384-well plate, using the instrumentations normally dedicated to fluorescence analysis in High Throughput Screening (HTS) activities, such as for example the FLIPR (Fluorometric Imaging Plate Reader) instrument

Optical modulation for optogenetic assays can be obtained in a miniaturized 384-well plate format using the FLIPR instrument.

we sought to determine if this optical modulation can be obtained also in a miniaturized format, such as a 384-well plate, using the instrumentations normally dedicated to fluorescence analysis in High Throughput Screening (HTS) activities, such as for example the FLIPR (Fluorometric Imaging Plate Reader) instrument

Stable, robust, and miniaturized cellular assays can be developed using different optogenetic tools and modulated by FLIPR LEDs in a 384-well format.

stable, robust and miniaturized cellular assays can be developed using different optogenetic tools, and efficiently modulated by the FLIPR instrument LEDs in a 384-well format

Stable, robust, and miniaturized cellular assays can be developed using different optogenetic tools and modulated by FLIPR LEDs in a 384-well format.

stable, robust and miniaturized cellular assays can be developed using different optogenetic tools, and efficiently modulated by the FLIPR instrument LEDs in a 384-well format

Stable, robust, and miniaturized cellular assays can be developed using different optogenetic tools and modulated by FLIPR LEDs in a 384-well format.

stable, robust and miniaturized cellular assays can be developed using different optogenetic tools, and efficiently modulated by the FLIPR instrument LEDs in a 384-well format

Stable, robust, and miniaturized cellular assays can be developed using different optogenetic tools and modulated by FLIPR LEDs in a 384-well format.

stable, robust and miniaturized cellular assays can be developed using different optogenetic tools, and efficiently modulated by the FLIPR instrument LEDs in a 384-well format

Stable, robust, and miniaturized cellular assays can be developed using different optogenetic tools and modulated by FLIPR LEDs in a 384-well format.

stable, robust and miniaturized cellular assays can be developed using different optogenetic tools, and efficiently modulated by the FLIPR instrument LEDs in a 384-well format

Stable, robust, and miniaturized cellular assays can be developed using different optogenetic tools and modulated by FLIPR LEDs in a 384-well format.

stable, robust and miniaturized cellular assays can be developed using different optogenetic tools, and efficiently modulated by the FLIPR instrument LEDs in a 384-well format

Stable, robust, and miniaturized cellular assays can be developed using different optogenetic tools and modulated by FLIPR LEDs in a 384-well format.

stable, robust and miniaturized cellular assays can be developed using different optogenetic tools, and efficiently modulated by the FLIPR instrument LEDs in a 384-well format

Channelrhodopsin-2 can be used to control the number and frequency of action potentials.

Using the naturally occurring algal protein Channelrhodopsin-2 (ChR2), a rapidly gated light-sensitive cation channel, the number and frequency of action potentials can be controlled.

Channelrhodopsin-2 can be used to control the number and frequency of action potentials.

Using the naturally occurring algal protein Channelrhodopsin-2 (ChR2), a rapidly gated light-sensitive cation channel, the number and frequency of action potentials can be controlled.

Channelrhodopsin-2 can be used to control the number and frequency of action potentials.

Using the naturally occurring algal protein Channelrhodopsin-2 (ChR2), a rapidly gated light-sensitive cation channel, the number and frequency of action potentials can be controlled.

Channelrhodopsin-2 can be used to control the number and frequency of action potentials.

Using the naturally occurring algal protein Channelrhodopsin-2 (ChR2), a rapidly gated light-sensitive cation channel, the number and frequency of action potentials can be controlled.

Channelrhodopsin-2 can be used to control the number and frequency of action potentials.

Using the naturally occurring algal protein Channelrhodopsin-2 (ChR2), a rapidly gated light-sensitive cation channel, the number and frequency of action potentials can be controlled.

Channelrhodopsin-2 can be used to control the number and frequency of action potentials.

Using the naturally occurring algal protein Channelrhodopsin-2 (ChR2), a rapidly gated light-sensitive cation channel, the number and frequency of action potentials can be controlled.

Channelrhodopsin-2 can be used to control the number and frequency of action potentials.

Using the naturally occurring algal protein Channelrhodopsin-2 (ChR2), a rapidly gated light-sensitive cation channel, the number and frequency of action potentials can be controlled.

bPAC adenylyl cyclase was used to modulate the HCN2 cyclic nucleotide gated channel in an optogenetic assay.

the HCN2 cyclic nucleotide gated (CNG) channel was modulated by the light activated bPAC adenylyl cyclase

bPAC adenylyl cyclase was used to modulate the HCN2 cyclic nucleotide gated channel in an optogenetic assay.

the HCN2 cyclic nucleotide gated (CNG) channel was modulated by the light activated bPAC adenylyl cyclase

bPAC adenylyl cyclase was used to modulate the HCN2 cyclic nucleotide gated channel in an optogenetic assay.

the HCN2 cyclic nucleotide gated (CNG) channel was modulated by the light activated bPAC adenylyl cyclase

bPAC adenylyl cyclase was used to modulate the HCN2 cyclic nucleotide gated channel in an optogenetic assay.

the HCN2 cyclic nucleotide gated (CNG) channel was modulated by the light activated bPAC adenylyl cyclase

bPAC adenylyl cyclase was used to modulate the HCN2 cyclic nucleotide gated channel in an optogenetic assay.

the HCN2 cyclic nucleotide gated (CNG) channel was modulated by the light activated bPAC adenylyl cyclase

bPAC adenylyl cyclase was used to modulate the HCN2 cyclic nucleotide gated channel in an optogenetic assay.

the HCN2 cyclic nucleotide gated (CNG) channel was modulated by the light activated bPAC adenylyl cyclase

bPAC adenylyl cyclase was used to modulate the HCN2 cyclic nucleotide gated channel in an optogenetic assay.

the HCN2 cyclic nucleotide gated (CNG) channel was modulated by the light activated bPAC adenylyl cyclase

Channelrhodopsin-2 was used to modulate the CaV1.3 calcium channel in an optogenetic assay.

the CaV1.3 calcium channel was modulated by the light-activated Channelrhodopsin-2

Channelrhodopsin-2 was used to modulate the CaV1.3 calcium channel in an optogenetic assay.

the CaV1.3 calcium channel was modulated by the light-activated Channelrhodopsin-2

Channelrhodopsin-2 was used to modulate the CaV1.3 calcium channel in an optogenetic assay.

the CaV1.3 calcium channel was modulated by the light-activated Channelrhodopsin-2

Channelrhodopsin-2 was used to modulate the CaV1.3 calcium channel in an optogenetic assay.

the CaV1.3 calcium channel was modulated by the light-activated Channelrhodopsin-2

Channelrhodopsin-2 was used to modulate the CaV1.3 calcium channel in an optogenetic assay.

the CaV1.3 calcium channel was modulated by the light-activated Channelrhodopsin-2

Channelrhodopsin-2 was used to modulate the CaV1.3 calcium channel in an optogenetic assay.

the CaV1.3 calcium channel was modulated by the light-activated Channelrhodopsin-2

Channelrhodopsin-2 provides a way to manipulate a single type of neuron while affecting no others.

The ChR2 provides a way to manipulate a single type of neuron while affecting no others, an unprecedented specificity.

Channelrhodopsin-2 provides a way to manipulate a single type of neuron while affecting no others.

The ChR2 provides a way to manipulate a single type of neuron while affecting no others, an unprecedented specificity.

Channelrhodopsin-2 provides a way to manipulate a single type of neuron while affecting no others.

The ChR2 provides a way to manipulate a single type of neuron while affecting no others, an unprecedented specificity.

Channelrhodopsin-2 provides a way to manipulate a single type of neuron while affecting no others.

The ChR2 provides a way to manipulate a single type of neuron while affecting no others, an unprecedented specificity.

Channelrhodopsin-2 provides a way to manipulate a single type of neuron while affecting no others.

The ChR2 provides a way to manipulate a single type of neuron while affecting no others, an unprecedented specificity.

Channelrhodopsin-2 provides a way to manipulate a single type of neuron while affecting no others.

The ChR2 provides a way to manipulate a single type of neuron while affecting no others, an unprecedented specificity.

Channelrhodopsin-2 provides a way to manipulate a single type of neuron while affecting no others.

The ChR2 provides a way to manipulate a single type of neuron while affecting no others, an unprecedented specificity.

The review context highlights optogenetic and chemogenetic tools as major approaches for manipulating genetically defined amygdala populations in fear-circuit studies.

ChR2 has been used to control neuronal activity in vitro and in vivo on short time scales and with exquisite anatomical precision.

ChR2 has been used by many groups to control neuronal activity, both in vitro and in vivo , on short time scales and with exquisite anatomical precision.

Optogenetic stimulation of spiral ganglion neurons restored auditory activity in deaf mice.

Furthermore, optogenetic stimulation of SGNs restored auditory activity in deaf mice.

Light-activated Gq protein-coupled opsins are described as a way to selectively activate astrocytes to explore the influence of gliotransmission on epileptic network function.

The influence of gliotransmission on epileptic network function is another topic of great interest that can be further explored by using light-activated Gq protein-coupled opsins for selective activation of astrocytes.

Light-activated Gq protein-coupled opsins are described as a way to selectively activate astrocytes to explore the influence of gliotransmission on epileptic network function.

The influence of gliotransmission on epileptic network function is another topic of great interest that can be further explored by using light-activated Gq protein-coupled opsins for selective activation of astrocytes.

Light-activated Gq protein-coupled opsins are described as a way to selectively activate astrocytes to explore the influence of gliotransmission on epileptic network function.

The influence of gliotransmission on epileptic network function is another topic of great interest that can be further explored by using light-activated Gq protein-coupled opsins for selective activation of astrocytes.

Light-activated Gq protein-coupled opsins are described as a way to selectively activate astrocytes to explore the influence of gliotransmission on epileptic network function.

The influence of gliotransmission on epileptic network function is another topic of great interest that can be further explored by using light-activated Gq protein-coupled opsins for selective activation of astrocytes.

Light-activated Gq protein-coupled opsins are described as a way to selectively activate astrocytes to explore the influence of gliotransmission on epileptic network function.

The influence of gliotransmission on epileptic network function is another topic of great interest that can be further explored by using light-activated Gq protein-coupled opsins for selective activation of astrocytes.

Light-activated Gq protein-coupled opsins are described as a way to selectively activate astrocytes to explore the influence of gliotransmission on epileptic network function.

The influence of gliotransmission on epileptic network function is another topic of great interest that can be further explored by using light-activated Gq protein-coupled opsins for selective activation of astrocytes.

Light-activated Gq protein-coupled opsins are described as a way to selectively activate astrocytes to explore the influence of gliotransmission on epileptic network function.

The influence of gliotransmission on epileptic network function is another topic of great interest that can be further explored by using light-activated Gq protein-coupled opsins for selective activation of astrocytes.

Channelrhodopsin-2, halorhodopsin, and archaerhodopsin-3 are presented as potent optogenetic candidates for controlling neuronal firing in models of epilepsy and for providing insights into neuronal network organization and synchronization.

The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization.

Channelrhodopsin-2, halorhodopsin, and archaerhodopsin-3 are presented as potent optogenetic candidates for controlling neuronal firing in models of epilepsy and for providing insights into neuronal network organization and synchronization.

The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization.

Channelrhodopsin-2, halorhodopsin, and archaerhodopsin-3 are presented as potent optogenetic candidates for controlling neuronal firing in models of epilepsy and for providing insights into neuronal network organization and synchronization.

The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization.

Channelrhodopsin-2, halorhodopsin, and archaerhodopsin-3 are presented as potent optogenetic candidates for controlling neuronal firing in models of epilepsy and for providing insights into neuronal network organization and synchronization.

The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization.

Channelrhodopsin-2, halorhodopsin, and archaerhodopsin-3 are presented as potent optogenetic candidates for controlling neuronal firing in models of epilepsy and for providing insights into neuronal network organization and synchronization.

The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization.

Channelrhodopsin-2, halorhodopsin, and archaerhodopsin-3 are presented as potent optogenetic candidates for controlling neuronal firing in models of epilepsy and for providing insights into neuronal network organization and synchronization.

The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization.

Channelrhodopsin-2, halorhodopsin, and archaerhodopsin-3 are presented as potent optogenetic candidates for controlling neuronal firing in models of epilepsy and for providing insights into neuronal network organization and synchronization.

The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization.

The optogenetic toolbox can be combined with juxtacellular recording and two-photon guided whole-cell recording to help identify specific cortical and hippocampal neuron subtypes altered in epileptic networks.

The ever-growing optogenetic toolbox can also be combined with emerging techniques that have greatly expanded our ability to record specific subtypes of cortical and hippocampal neurons in awake behaving animals such as juxtacellular recording and two-photon guided whole-cell recording, to identify the specific subtypes of neurons that are altered in epileptic networks.

The optogenetic toolbox can be combined with juxtacellular recording and two-photon guided whole-cell recording to help identify specific cortical and hippocampal neuron subtypes altered in epileptic networks.

The ever-growing optogenetic toolbox can also be combined with emerging techniques that have greatly expanded our ability to record specific subtypes of cortical and hippocampal neurons in awake behaving animals such as juxtacellular recording and two-photon guided whole-cell recording, to identify the specific subtypes of neurons that are altered in epileptic networks.

The optogenetic toolbox can be combined with juxtacellular recording and two-photon guided whole-cell recording to help identify specific cortical and hippocampal neuron subtypes altered in epileptic networks.

The ever-growing optogenetic toolbox can also be combined with emerging techniques that have greatly expanded our ability to record specific subtypes of cortical and hippocampal neurons in awake behaving animals such as juxtacellular recording and two-photon guided whole-cell recording, to identify the specific subtypes of neurons that are altered in epileptic networks.

The optogenetic toolbox can be combined with juxtacellular recording and two-photon guided whole-cell recording to help identify specific cortical and hippocampal neuron subtypes altered in epileptic networks.

The ever-growing optogenetic toolbox can also be combined with emerging techniques that have greatly expanded our ability to record specific subtypes of cortical and hippocampal neurons in awake behaving animals such as juxtacellular recording and two-photon guided whole-cell recording, to identify the specific subtypes of neurons that are altered in epileptic networks.

The optogenetic toolbox can be combined with juxtacellular recording and two-photon guided whole-cell recording to help identify specific cortical and hippocampal neuron subtypes altered in epileptic networks.

The ever-growing optogenetic toolbox can also be combined with emerging techniques that have greatly expanded our ability to record specific subtypes of cortical and hippocampal neurons in awake behaving animals such as juxtacellular recording and two-photon guided whole-cell recording, to identify the specific subtypes of neurons that are altered in epileptic networks.

The optogenetic toolbox can be combined with juxtacellular recording and two-photon guided whole-cell recording to help identify specific cortical and hippocampal neuron subtypes altered in epileptic networks.

The ever-growing optogenetic toolbox can also be combined with emerging techniques that have greatly expanded our ability to record specific subtypes of cortical and hippocampal neurons in awake behaving animals such as juxtacellular recording and two-photon guided whole-cell recording, to identify the specific subtypes of neurons that are altered in epileptic networks.

The optogenetic toolbox can be combined with juxtacellular recording and two-photon guided whole-cell recording to help identify specific cortical and hippocampal neuron subtypes altered in epileptic networks.

The ever-growing optogenetic toolbox can also be combined with emerging techniques that have greatly expanded our ability to record specific subtypes of cortical and hippocampal neurons in awake behaving animals such as juxtacellular recording and two-photon guided whole-cell recording, to identify the specific subtypes of neurons that are altered in epileptic networks.

Virus-mediated expression of a more light-sensitive ChR2 variant in spiral ganglion neurons reduced the amount of light required for responses and allowed neuronal spiking up to 60 Hz.

Virus-mediated expression of a ChR2 variant with greater light sensitivity in SGNs reduced the amount of light required for responses and allowed neuronal spiking following stimulation up to 60 Hz.

Optogenetic stimulation of spiral ganglion neurons activated the auditory pathway.

Optogenetic stimulation of spiral ganglion neurons (SGNs) activated the auditory pathway, as demonstrated by recordings of single neuron and neuronal population responses.

Optogenetic tools allow rapid and reversible suppression of epileptic EEG activity upon photoactivation.

Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation.

Optogenetic tools allow rapid and reversible suppression of epileptic EEG activity upon photoactivation.

Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation.

Optogenetic tools allow rapid and reversible suppression of epileptic EEG activity upon photoactivation.

Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation.

Optogenetic tools allow rapid and reversible suppression of epileptic EEG activity upon photoactivation.

Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation.

Optogenetic tools allow rapid and reversible suppression of epileptic EEG activity upon photoactivation.

Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation.

Optogenetic tools allow rapid and reversible suppression of epileptic EEG activity upon photoactivation.

Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation.

Optogenetic tools allow rapid and reversible suppression of epileptic EEG activity upon photoactivation.

Finally, optogenetic tools allow rapid and reversible suppression of epileptic electroencephalography (EEG) activity upon photoactivation.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, including interneuron subclasses, to study activity patterns in distinct brain states and dissect roles in synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, or subclasses of interneurons, to study their activity patterns in distinct brain-states in vivo and to dissect their role in generation of synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, including interneuron subclasses, to study activity patterns in distinct brain states and dissect roles in synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, or subclasses of interneurons, to study their activity patterns in distinct brain-states in vivo and to dissect their role in generation of synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, including interneuron subclasses, to study activity patterns in distinct brain states and dissect roles in synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, or subclasses of interneurons, to study their activity patterns in distinct brain-states in vivo and to dissect their role in generation of synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, including interneuron subclasses, to study activity patterns in distinct brain states and dissect roles in synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, or subclasses of interneurons, to study their activity patterns in distinct brain-states in vivo and to dissect their role in generation of synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, including interneuron subclasses, to study activity patterns in distinct brain states and dissect roles in synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, or subclasses of interneurons, to study their activity patterns in distinct brain-states in vivo and to dissect their role in generation of synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, including interneuron subclasses, to study activity patterns in distinct brain states and dissect roles in synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, or subclasses of interneurons, to study their activity patterns in distinct brain-states in vivo and to dissect their role in generation of synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, including interneuron subclasses, to study activity patterns in distinct brain states and dissect roles in synchrony and seizures.

Opsins allow selective activation of excitatory neurons and inhibitory interneurons, or subclasses of interneurons, to study their activity patterns in distinct brain-states in vivo and to dissect their role in generation of synchrony and seizures.

A light-activated transgene system is a more recently developed optogenetic tool discussed by the source.

and a light-activated transgene system.

Opsin/G protein-coupled receptor chimeric molecules are more recently developed optogenetic tools discussed by the source.

In addition, we describe more recently developed tools such as opsin/G protein-coupled receptor chimeric molecules

ChR2 is the photosensitive protein most commonly employed in optogenetics.

We focus especially on the channelrhodopsin protein ChR2, the photosensitive protein most commonly employed in optogenetics.

Optogenetic stimulation allows arbitrary stimulation of opsin-expressing brain regions, enabling brain mapping independent of behavior or sensory processing.

The optogenetic seizure-like afterdischarge model was advantageous for reproducibility and artifact-free electrophysiological observations.

Hippocampal photostimulation of ChR2-expressing rodents successfully induced seizure-like afterdischarges in both transgenic rats and wild-type rats transfected with AAV vectors carrying ChR2.

With KENGE-tet-based optogenetic mice, in vivo manipulation of nonexcitable glial cells is possible in addition to neurons.

In addition to neurons, manipulations of the activities of nonexcitable glial cells in vivo have also proved possible.

A recent report using KENGE-tet found that selective optogenetic stimulation of glia can lead to glutamate release, synaptic plasticity, and accelerated cerebellar-modulated motor learning.

A recent report that used the KENGE-tet has shown that the selective optogenetic stimulation of glia can lead to the release of glutamate as a gliotransmitter, synaptic plasticity, and the acceleration of cerebellar-modulated motor learning.

Channelrhodopsin-2 can be genetically expressed in mammalian brain cells to allow optical control of cell activity.

channelrhodopsin-2, that are found in microorganisms can now be genetically expressed in mammalian brain cells, allowing experimenters to optically control cell activity at will

Red-shifted organic voltage-sensitive dyes permit high temporal resolution imaging that is spectrally separated from Channelrhodopsin-2 activation.

Long-term in vivo optogenetic studies in this review context rely on implantable optical-fiber strategies for light delivery.

A single induced afterdischarge produced c-Fos evidence of neuronal activation across the entire hippocampus.

VSD maps stimulated by ChR2 were dependent on intracortical synaptic activity and reflected circuits used for sensory processing.

The computational modeling technique was demonstrated using channelrhodopsin-2 and halorhodopsin as examples of optical activation and silencing mechanisms.

It was demonstrated on the example of a two classical mechanisms for cells optical activation and silencing: channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR).

The computational modeling technique was demonstrated using channelrhodopsin-2 and halorhodopsin as examples of optical activation and silencing mechanisms.

It was demonstrated on the example of a two classical mechanisms for cells optical activation and silencing: channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR).

The computational modeling technique was demonstrated using channelrhodopsin-2 and halorhodopsin as examples of optical activation and silencing mechanisms.

It was demonstrated on the example of a two classical mechanisms for cells optical activation and silencing: channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR).

The computational modeling technique was demonstrated using channelrhodopsin-2 and halorhodopsin as examples of optical activation and silencing mechanisms.

It was demonstrated on the example of a two classical mechanisms for cells optical activation and silencing: channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR).

The computational modeling technique was demonstrated using channelrhodopsin-2 and halorhodopsin as examples of optical activation and silencing mechanisms.

It was demonstrated on the example of a two classical mechanisms for cells optical activation and silencing: channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR).

The computational modeling technique was demonstrated using channelrhodopsin-2 and halorhodopsin as examples of optical activation and silencing mechanisms.

It was demonstrated on the example of a two classical mechanisms for cells optical activation and silencing: channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR).

The computational modeling technique was demonstrated using channelrhodopsin-2 and halorhodopsin as examples of optical activation and silencing mechanisms.

It was demonstrated on the example of a two classical mechanisms for cells optical activation and silencing: channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR).

Projection-specific optogenetic manipulation is presented as a central strategy for dissecting stress-related circuitry.

KENGE-tet generated a repertoire of transgenic mice expressing a highly light-sensitive channelrhodopsin-2 mutant at levels sufficient to stimulate multiple cell types.

KENGE-tet method, which has generated a repertoire of transgenic mice that express levels of the highly light-sensitive channelrhodopsin-2 mutant that are sufficient to stimulate multiple cell types

The paper presents a generalised computational modeling technique for various optogenetic mechanisms implemented in the NEURON simulation environment.

Here we present a generalised computational modeling technique for various types of optogenetic mechanisms, which was implemented in the NEURON simulation environment.

The paper presents a generalised computational modeling technique for various optogenetic mechanisms implemented in the NEURON simulation environment.

Here we present a generalised computational modeling technique for various types of optogenetic mechanisms, which was implemented in the NEURON simulation environment.

The paper presents a generalised computational modeling technique for various optogenetic mechanisms implemented in the NEURON simulation environment.

Here we present a generalised computational modeling technique for various types of optogenetic mechanisms, which was implemented in the NEURON simulation environment.

The paper presents a generalised computational modeling technique for various optogenetic mechanisms implemented in the NEURON simulation environment.

Here we present a generalised computational modeling technique for various types of optogenetic mechanisms, which was implemented in the NEURON simulation environment.

The paper presents a generalised computational modeling technique for various optogenetic mechanisms implemented in the NEURON simulation environment.

Here we present a generalised computational modeling technique for various types of optogenetic mechanisms, which was implemented in the NEURON simulation environment.

The paper presents a generalised computational modeling technique for various optogenetic mechanisms implemented in the NEURON simulation environment.

Here we present a generalised computational modeling technique for various types of optogenetic mechanisms, which was implemented in the NEURON simulation environment.

The paper presents a generalised computational modeling technique for various optogenetic mechanisms implemented in the NEURON simulation environment.

Here we present a generalised computational modeling technique for various types of optogenetic mechanisms, which was implemented in the NEURON simulation environment.

The paper developed a novel in vivo optogenetic model of seizure-like afterdischarge in the rodent hippocampus.

Granger causality analysis of hippocampal LFPs showed bidirectional but asymmetric signal flow along the septo-temporal axis during seizure-like afterdischarges.

Pulse frequencies of 10 and 20 Hz with a 0.05 duty ratio were optimal for afterdischarge induction.

Opsin-based activation allows investigation of connectivity with spatial resolution on the order of single neurons and temporal resolution on the order of milliseconds.

In the modeled layer 5 cortical pyramidal neuron, whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and can silence the cell even when driving input is present.

We show that whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and is able to silence the cell even when driving input is present.

In the modeled layer 5 cortical pyramidal neuron, whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and can silence the cell even when driving input is present.

We show that whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and is able to silence the cell even when driving input is present.

In the modeled layer 5 cortical pyramidal neuron, whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and can silence the cell even when driving input is present.

We show that whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and is able to silence the cell even when driving input is present.

In the modeled layer 5 cortical pyramidal neuron, whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and can silence the cell even when driving input is present.

We show that whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and is able to silence the cell even when driving input is present.

In the modeled layer 5 cortical pyramidal neuron, whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and can silence the cell even when driving input is present.

We show that whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and is able to silence the cell even when driving input is present.

In the modeled layer 5 cortical pyramidal neuron, whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and can silence the cell even when driving input is present.

We show that whole-cell illumination of halorhodopsin most effectively hyperpolarizes the neuron and is able to silence the cell even when driving input is present.

When channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the neural response is modulated toward depolarization.

However, when channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the response is modulated with a balance towards depolarization.

When channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the neural response is modulated toward depolarization.

However, when channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the response is modulated with a balance towards depolarization.

When channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the neural response is modulated toward depolarization.

However, when channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the response is modulated with a balance towards depolarization.

When channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the neural response is modulated toward depolarization.

However, when channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the response is modulated with a balance towards depolarization.

When channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the neural response is modulated toward depolarization.

However, when channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the response is modulated with a balance towards depolarization.

When channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the neural response is modulated toward depolarization.

However, when channelrhodopsin-2 and halorhodopsin are concurrently active, the relative location of each illumination determines whether the response is modulated with a balance towards depolarization.

State-space analysis of causality and coherence identified three discrete states of seizure-like afterdischarge: resting, initiation with dominant septal-to-temporal causality, and termination with dominant temporal-to-septal causality.

The review discusses promoter-based targeting such as CaMKIIα to enrich opsin delivery to selected neuronal populations.

The review discusses both excitatory and inhibitory optogenetic actuators for causal manipulation of stress-related neural circuits.

Channelrhodopsin-2 was used as an optogenetic tag to identify PV+ and PV- neurons in vivo in transgenic mice.

We used channelrhodopsin-2 (ChR2) as an optogenetic tag to identify PV+ and PV- neurons in vivo in transgenic mice.

A single 200 ms light pulse delivered after each self-initiated nose poke was sufficient to cause operant reinforcement.

When a single light pulse followed each self-initiated nose poke, it was sufficient in itself to cause operant reinforcement.

Optical stimulation of genetically targeted VTA dopamine neurons increased locomotion and contralateral rotations when delivered according to a predetermined pattern in separate sessions.

when optical stimulation was delivered in separate sessions according to a predetermined pattern, it increased locomotion and contralateral rotations

A bicistronic expression cassette with GFP helps identify the correct expression pattern.

A bicistronic expression cassette with GFP helps to identify the correct expression pattern

A bicistronic expression cassette with GFP helps identify the correct expression pattern.

A bicistronic expression cassette with GFP helps to identify the correct expression pattern

A bicistronic expression cassette with GFP helps identify the correct expression pattern.

A bicistronic expression cassette with GFP helps to identify the correct expression pattern

A bicistronic expression cassette with GFP helps identify the correct expression pattern.

A bicistronic expression cassette with GFP helps to identify the correct expression pattern

A bicistronic expression cassette with GFP helps identify the correct expression pattern.

A bicistronic expression cassette with GFP helps to identify the correct expression pattern

A bicistronic expression cassette with GFP helps identify the correct expression pattern.

A bicistronic expression cassette with GFP helps to identify the correct expression pattern

A bicistronic expression cassette with GFP helps identify the correct expression pattern.

A bicistronic expression cassette with GFP helps to identify the correct expression pattern

Optically induced operant and locomotor behaviors were tightly correlated with the number of VTA dopamine neurons expressing ChR2.

All three of the optically induced operant and locomotor behaviors were tightly correlated with the number of VTA dopamine neurons that expressed ChR2

Success of the conditional single-neuron Channelrhodopsin-2 expression method depends on precise knowledge of individual promoter expression patterns and on relative expression levels of recombinase and Channelrhodopsin-2.

Success of this method depends on precise knowledge of the individual promoters' expression patterns and on relative expression levels of recombinase and ChR2

Success of the conditional single-neuron Channelrhodopsin-2 expression method depends on precise knowledge of individual promoter expression patterns and on relative expression levels of recombinase and Channelrhodopsin-2.

Success of this method depends on precise knowledge of the individual promoters' expression patterns and on relative expression levels of recombinase and ChR2

Success of the conditional single-neuron Channelrhodopsin-2 expression method depends on precise knowledge of individual promoter expression patterns and on relative expression levels of recombinase and Channelrhodopsin-2.

Success of this method depends on precise knowledge of the individual promoters' expression patterns and on relative expression levels of recombinase and ChR2

Success of the conditional single-neuron Channelrhodopsin-2 expression method depends on precise knowledge of individual promoter expression patterns and on relative expression levels of recombinase and Channelrhodopsin-2.

Success of this method depends on precise knowledge of the individual promoters' expression patterns and on relative expression levels of recombinase and ChR2

Success of the conditional single-neuron Channelrhodopsin-2 expression method depends on precise knowledge of individual promoter expression patterns and on relative expression levels of recombinase and Channelrhodopsin-2.

Success of this method depends on precise knowledge of the individual promoters' expression patterns and on relative expression levels of recombinase and ChR2

Success of the conditional single-neuron Channelrhodopsin-2 expression method depends on precise knowledge of individual promoter expression patterns and on relative expression levels of recombinase and Channelrhodopsin-2.

Success of this method depends on precise knowledge of the individual promoters' expression patterns and on relative expression levels of recombinase and ChR2

The authors show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons.

Here we show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons

The authors show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons.

Here we show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons

The authors show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons.

Here we show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons

The authors show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons.

Here we show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons

The authors show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons.

Here we show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons

The authors show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons.

Here we show specific expression in the AVA reverse command neurons and the aversive polymodal sensory ASH neurons

ChR2 responds to blue light to induce neuronal firing via cation influx.

ChR2 responds to blue light to induce neuronal firing via cation influx

NpHR responds to yellow light to inhibit neuronal activity via chloride influx.

NpHR responds to yellow light to inhibit neuronal activity via Cl- influx

The authors used Cre or FLP recombinases with conditional Channelrhodopsin-2 expression at the intersection of two promoter expression domains to restrict expression to the cell of interest.

we adopted the use of Cre or FLP recombinases and conditional ChR2 expression at the intersection of two promoter expression domains, i.e. in the cell of interest only

The authors used Cre or FLP recombinases with conditional Channelrhodopsin-2 expression at the intersection of two promoter expression domains to restrict expression to the cell of interest.

we adopted the use of Cre or FLP recombinases and conditional ChR2 expression at the intersection of two promoter expression domains, i.e. in the cell of interest only

The authors used Cre or FLP recombinases with conditional Channelrhodopsin-2 expression at the intersection of two promoter expression domains to restrict expression to the cell of interest.

we adopted the use of Cre or FLP recombinases and conditional ChR2 expression at the intersection of two promoter expression domains, i.e. in the cell of interest only

The authors used Cre or FLP recombinases with conditional Channelrhodopsin-2 expression at the intersection of two promoter expression domains to restrict expression to the cell of interest.

we adopted the use of Cre or FLP recombinases and conditional ChR2 expression at the intersection of two promoter expression domains, i.e. in the cell of interest only

The authors used Cre or FLP recombinases with conditional Channelrhodopsin-2 expression at the intersection of two promoter expression domains to restrict expression to the cell of interest.

we adopted the use of Cre or FLP recombinases and conditional ChR2 expression at the intersection of two promoter expression domains, i.e. in the cell of interest only

The authors used Cre or FLP recombinases with conditional Channelrhodopsin-2 expression at the intersection of two promoter expression domains to restrict expression to the cell of interest.

we adopted the use of Cre or FLP recombinases and conditional ChR2 expression at the intersection of two promoter expression domains, i.e. in the cell of interest only

In source material connected to this review, ChR2 and NpHR are explicit optogenetic actuators used to interrogate dopamine circuits, while FSCV is an explicit paired measurement method for dopamine release dynamics.

Explicitly supported related components/tools include ChR2, NpHR, fast-scan cyclic voltammetry (FSCV), TH-Cre, DAT-Cre, and recombinase-driver rat lines.

The source synthesizes early optogenetic circuit-dissection studies of emotional valence and motivated behaviors, emphasizing ChR2, NpHR/eNpHR3.0, and projection-specific manipulations.

The review synthesizes early optogenetic circuit-dissection work across mesolimbic dopamine, striatum, hypothalamus, and amygdala, emphasizing tools such as ChR2 and NpHR/eNpHR3.0 and projection-specific manipulations.

A 200 ms optogenetic activation of genetically targeted VTA dopamine neurons was sufficient to mimic transient natural reward-associated dopamine activation.

We mimicked the transient activation of dopamine neurons that occurs in response to natural reward by applying a light pulse of 200 ms in VTA.

Selective genetic targeting is a central enabling component in dopamine optogenetics, with TH-Cre, DAT-Cre, and recombinase-driver rat lines identified as relevant targeting tools in source material connected to this review.

Explicitly supported related components/tools include ChR2, NpHR, fast-scan cyclic voltammetry (FSCV), TH-Cre, DAT-Cre, and recombinase-driver rat lines.

Channelrhodopsin-2 is presented in the supplied evidence scaffold as an optogenetic actuator enabling causal circuit perturbation in studies aligned to this review's scope.

Channelrhodopsin-2 and PAC α expressed in individual olfactory receptor neurons of Drosophila larvae allow stimulation of individual receptor neurons by light.

Both channelrhodopsin-2 and the photosensitive adenylyl cyclase PAC α in individual olfactory receptor neurons (ORNs) of the olfactory system of Drosophila larvae allows stimulating individual receptor neurons by light.

The reviewed remote-control tools differ in effect direction, onset and offset kinetics, spatial resolution, and invasiveness.

None of the reviewed neuronal remote-control tools is perfect, and each has advantages and disadvantages.

The reviewed tools use light, peptides, and small molecules to primarily activate ion channels and GPCRs, thereby activating or inhibiting neuronal firing.

Remote bidirectional manipulation of neuronal electrical and chemical signaling with high spatiotemporal precision is presented as an ideal approach for linking neural activity to behavior.

The review compares channelrhodopsin variants using seven key properties that influence their effectiveness as research tools: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response, and membrane trafficking.

In this review, the seven following key properties of ChRs that have significant influences on their effectiveness as research tools are examined: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response and membrane trafficking.

The review compares channelrhodopsin variants using seven key properties that influence their effectiveness as research tools: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response, and membrane trafficking.

In this review, the seven following key properties of ChRs that have significant influences on their effectiveness as research tools are examined: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response and membrane trafficking.

The review compares channelrhodopsin variants using seven key properties that influence their effectiveness as research tools: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response, and membrane trafficking.

In this review, the seven following key properties of ChRs that have significant influences on their effectiveness as research tools are examined: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response and membrane trafficking.

The review compares channelrhodopsin variants using seven key properties that influence their effectiveness as research tools: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response, and membrane trafficking.

In this review, the seven following key properties of ChRs that have significant influences on their effectiveness as research tools are examined: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response and membrane trafficking.

The review compares channelrhodopsin variants using seven key properties that influence their effectiveness as research tools: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response, and membrane trafficking.

In this review, the seven following key properties of ChRs that have significant influences on their effectiveness as research tools are examined: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response and membrane trafficking.

The review compares channelrhodopsin variants using seven key properties that influence their effectiveness as research tools: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response, and membrane trafficking.

In this review, the seven following key properties of ChRs that have significant influences on their effectiveness as research tools are examined: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response and membrane trafficking.

The review compares channelrhodopsin variants using seven key properties that influence their effectiveness as research tools: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response, and membrane trafficking.

In this review, the seven following key properties of ChRs that have significant influences on their effectiveness as research tools are examined: conductance, selectivity, kinetics, desensitization, light sensitivity, spectral response and membrane trafficking.

Chimeragenesis, mutagenesis, and bioinformatic approaches have introduced additional channelrhodopsin variants including ChR2/H134R, ChETA, VChR1, VChR2, ChR2/C128X/D156A, ChD, ChEF, and I170V.

Subsequent chimeragenesis, mutagenesis and bioinformatic approaches have introduced additional ChR variants, such as channelrhodopsin-2 with H134R mutation (ChR2/H134R), channelrhodopsin-2 with E123T mutation (ChETA), Volvox carteri channelrhodopsin-1 (VChR1), Volvox carteri channelrhodopsin-2 (VChR2), channelrhodopsin-2 with C128 or D156A mutations (ChR2/C128X/D156A), chimera D (ChD), chimera EF (ChEF) and chimera EF with I170V mutation (I170V).

Chimeragenesis, mutagenesis, and bioinformatic approaches have introduced additional channelrhodopsin variants including ChR2/H134R, ChETA, VChR1, VChR2, ChR2/C128X/D156A, ChD, ChEF, and I170V.

Subsequent chimeragenesis, mutagenesis and bioinformatic approaches have introduced additional ChR variants, such as channelrhodopsin-2 with H134R mutation (ChR2/H134R), channelrhodopsin-2 with E123T mutation (ChETA), Volvox carteri channelrhodopsin-1 (VChR1), Volvox carteri channelrhodopsin-2 (VChR2), channelrhodopsin-2 with C128 or D156A mutations (ChR2/C128X/D156A), chimera D (ChD), chimera EF (ChEF) and chimera EF with I170V mutation (I170V).

Chimeragenesis, mutagenesis, and bioinformatic approaches have introduced additional channelrhodopsin variants including ChR2/H134R, ChETA, VChR1, VChR2, ChR2/C128X/D156A, ChD, ChEF, and I170V.

Subsequent chimeragenesis, mutagenesis and bioinformatic approaches have introduced additional ChR variants, such as channelrhodopsin-2 with H134R mutation (ChR2/H134R), channelrhodopsin-2 with E123T mutation (ChETA), Volvox carteri channelrhodopsin-1 (VChR1), Volvox carteri channelrhodopsin-2 (VChR2), channelrhodopsin-2 with C128 or D156A mutations (ChR2/C128X/D156A), chimera D (ChD), chimera EF (ChEF) and chimera EF with I170V mutation (I170V).

Chimeragenesis, mutagenesis, and bioinformatic approaches have introduced additional channelrhodopsin variants including ChR2/H134R, ChETA, VChR1, VChR2, ChR2/C128X/D156A, ChD, ChEF, and I170V.

Subsequent chimeragenesis, mutagenesis and bioinformatic approaches have introduced additional ChR variants, such as channelrhodopsin-2 with H134R mutation (ChR2/H134R), channelrhodopsin-2 with E123T mutation (ChETA), Volvox carteri channelrhodopsin-1 (VChR1), Volvox carteri channelrhodopsin-2 (VChR2), channelrhodopsin-2 with C128 or D156A mutations (ChR2/C128X/D156A), chimera D (ChD), chimera EF (ChEF) and chimera EF with I170V mutation (I170V).

Chimeragenesis, mutagenesis, and bioinformatic approaches have introduced additional channelrhodopsin variants including ChR2/H134R, ChETA, VChR1, VChR2, ChR2/C128X/D156A, ChD, ChEF, and I170V.

Subsequent chimeragenesis, mutagenesis and bioinformatic approaches have introduced additional ChR variants, such as channelrhodopsin-2 with H134R mutation (ChR2/H134R), channelrhodopsin-2 with E123T mutation (ChETA), Volvox carteri channelrhodopsin-1 (VChR1), Volvox carteri channelrhodopsin-2 (VChR2), channelrhodopsin-2 with C128 or D156A mutations (ChR2/C128X/D156A), chimera D (ChD), chimera EF (ChEF) and chimera EF with I170V mutation (I170V).

Chimeragenesis, mutagenesis, and bioinformatic approaches have introduced additional channelrhodopsin variants including ChR2/H134R, ChETA, VChR1, VChR2, ChR2/C128X/D156A, ChD, ChEF, and I170V.

Subsequent chimeragenesis, mutagenesis and bioinformatic approaches have introduced additional ChR variants, such as channelrhodopsin-2 with H134R mutation (ChR2/H134R), channelrhodopsin-2 with E123T mutation (ChETA), Volvox carteri channelrhodopsin-1 (VChR1), Volvox carteri channelrhodopsin-2 (VChR2), channelrhodopsin-2 with C128 or D156A mutations (ChR2/C128X/D156A), chimera D (ChD), chimera EF (ChEF) and chimera EF with I170V mutation (I170V).

Chimeragenesis, mutagenesis, and bioinformatic approaches have introduced additional channelrhodopsin variants including ChR2/H134R, ChETA, VChR1, VChR2, ChR2/C128X/D156A, ChD, ChEF, and I170V.

Subsequent chimeragenesis, mutagenesis and bioinformatic approaches have introduced additional ChR variants, such as channelrhodopsin-2 with H134R mutation (ChR2/H134R), channelrhodopsin-2 with E123T mutation (ChETA), Volvox carteri channelrhodopsin-1 (VChR1), Volvox carteri channelrhodopsin-2 (VChR2), channelrhodopsin-2 with C128 or D156A mutations (ChR2/C128X/D156A), chimera D (ChD), chimera EF (ChEF) and chimera EF with I170V mutation (I170V).

Channelrhodopsins are light-activated channels from algae that function as fast sensors to visible light for phototaxis.

Channelrhodopsins (ChRs) are light-activated channels from algae that provide these organisms with fast sensors to visible light for phototaxis.

Channelrhodopsins are light-activated channels from algae that function as fast sensors to visible light for phototaxis.

Channelrhodopsins (ChRs) are light-activated channels from algae that provide these organisms with fast sensors to visible light for phototaxis.

Channelrhodopsins are light-activated channels from algae that function as fast sensors to visible light for phototaxis.

Channelrhodopsins (ChRs) are light-activated channels from algae that provide these organisms with fast sensors to visible light for phototaxis.

Channelrhodopsins are light-activated channels from algae that function as fast sensors to visible light for phototaxis.

Channelrhodopsins (ChRs) are light-activated channels from algae that provide these organisms with fast sensors to visible light for phototaxis.

Channelrhodopsins are light-activated channels from algae that function as fast sensors to visible light for phototaxis.

Channelrhodopsins (ChRs) are light-activated channels from algae that provide these organisms with fast sensors to visible light for phototaxis.

Channelrhodopsins are light-activated channels from algae that function as fast sensors to visible light for phototaxis.

Channelrhodopsins (ChRs) are light-activated channels from algae that provide these organisms with fast sensors to visible light for phototaxis.

Channelrhodopsins are light-activated channels from algae that function as fast sensors to visible light for phototaxis.

Channelrhodopsins (ChRs) are light-activated channels from algae that provide these organisms with fast sensors to visible light for phototaxis.

The review summarizes valuable qualities and deficits of each channelrhodopsin variant and discusses optimal uses and potential future improvements of channelrhodopsins as optogenetic tools.

Using this information, valuable qualities and deficits of each ChR variant are summarized. Optimal uses and potential future improvements of ChRs as optogenetic tools are also discussed.

The review summarizes valuable qualities and deficits of each channelrhodopsin variant and discusses optimal uses and potential future improvements of channelrhodopsins as optogenetic tools.

Using this information, valuable qualities and deficits of each ChR variant are summarized. Optimal uses and potential future improvements of ChRs as optogenetic tools are also discussed.

The review summarizes valuable qualities and deficits of each channelrhodopsin variant and discusses optimal uses and potential future improvements of channelrhodopsins as optogenetic tools.

Using this information, valuable qualities and deficits of each ChR variant are summarized. Optimal uses and potential future improvements of ChRs as optogenetic tools are also discussed.

The review summarizes valuable qualities and deficits of each channelrhodopsin variant and discusses optimal uses and potential future improvements of channelrhodopsins as optogenetic tools.

Using this information, valuable qualities and deficits of each ChR variant are summarized. Optimal uses and potential future improvements of ChRs as optogenetic tools are also discussed.

The review summarizes valuable qualities and deficits of each channelrhodopsin variant and discusses optimal uses and potential future improvements of channelrhodopsins as optogenetic tools.

Using this information, valuable qualities and deficits of each ChR variant are summarized. Optimal uses and potential future improvements of ChRs as optogenetic tools are also discussed.

The review summarizes valuable qualities and deficits of each channelrhodopsin variant and discusses optimal uses and potential future improvements of channelrhodopsins as optogenetic tools.

Using this information, valuable qualities and deficits of each ChR variant are summarized. Optimal uses and potential future improvements of ChRs as optogenetic tools are also discussed.

The review summarizes valuable qualities and deficits of each channelrhodopsin variant and discusses optimal uses and potential future improvements of channelrhodopsins as optogenetic tools.

Using this information, valuable qualities and deficits of each ChR variant are summarized. Optimal uses and potential future improvements of ChRs as optogenetic tools are also discussed.

Channelrhodopsin-2 has been used as a research tool to depolarize membranes of excitable cells with light.

Since its discovery, channelrhodopsin-2 (ChR2) has been used as a research tool to depolarize membranes of excitable cells with light.

Channelrhodopsin-2 has been used as a research tool to depolarize membranes of excitable cells with light.

Since its discovery, channelrhodopsin-2 (ChR2) has been used as a research tool to depolarize membranes of excitable cells with light.

Channelrhodopsin-2 has been used as a research tool to depolarize membranes of excitable cells with light.

Since its discovery, channelrhodopsin-2 (ChR2) has been used as a research tool to depolarize membranes of excitable cells with light.

Channelrhodopsin-2 has been used as a research tool to depolarize membranes of excitable cells with light.

Since its discovery, channelrhodopsin-2 (ChR2) has been used as a research tool to depolarize membranes of excitable cells with light.

Channelrhodopsin-2 has been used as a research tool to depolarize membranes of excitable cells with light.

Since its discovery, channelrhodopsin-2 (ChR2) has been used as a research tool to depolarize membranes of excitable cells with light.

Channelrhodopsin-2 has been used as a research tool to depolarize membranes of excitable cells with light.

Since its discovery, channelrhodopsin-2 (ChR2) has been used as a research tool to depolarize membranes of excitable cells with light.

Channelrhodopsin-2 has been used as a research tool to depolarize membranes of excitable cells with light.

Since its discovery, channelrhodopsin-2 (ChR2) has been used as a research tool to depolarize membranes of excitable cells with light.

The study used a transgenic rat expressing ChR2 specifically in retinal ganglion cells under the regulation of a Thy-1.2 promoter.

by using a transgenic rat expressing ChR2 specifically in the RGCs under the regulation of a Thy-1.2 promoter

The study used a transgenic rat expressing ChR2 specifically in retinal ganglion cells under the regulation of a Thy-1.2 promoter.

by using a transgenic rat expressing ChR2 specifically in the RGCs under the regulation of a Thy-1.2 promoter

The study used a transgenic rat expressing ChR2 specifically in retinal ganglion cells under the regulation of a Thy-1.2 promoter.

by using a transgenic rat expressing ChR2 specifically in the RGCs under the regulation of a Thy-1.2 promoter

The study used a transgenic rat expressing ChR2 specifically in retinal ganglion cells under the regulation of a Thy-1.2 promoter.

by using a transgenic rat expressing ChR2 specifically in the RGCs under the regulation of a Thy-1.2 promoter

The study used a transgenic rat expressing ChR2 specifically in retinal ganglion cells under the regulation of a Thy-1.2 promoter.

by using a transgenic rat expressing ChR2 specifically in the RGCs under the regulation of a Thy-1.2 promoter

The study used a transgenic rat expressing ChR2 specifically in retinal ganglion cells under the regulation of a Thy-1.2 promoter.

by using a transgenic rat expressing ChR2 specifically in the RGCs under the regulation of a Thy-1.2 promoter

After degeneration of native photoreceptors, transgenic rats showed enhanced optomotor contrast sensitivity for low-spatial-frequency visual stimuli compared with wild-type-like baseline similarity.

Although the contrast sensitivities of the optomotor responses of transgenic rats were similar to those observed in the wild-type rats, they were enhanced for visual stimuli of low-spatial frequency after the degeneration of native photoreceptors.

After degeneration of native photoreceptors, transgenic rats showed enhanced optomotor contrast sensitivity for low-spatial-frequency visual stimuli compared with wild-type-like baseline similarity.

Although the contrast sensitivities of the optomotor responses of transgenic rats were similar to those observed in the wild-type rats, they were enhanced for visual stimuli of low-spatial frequency after the degeneration of native photoreceptors.

After degeneration of native photoreceptors, transgenic rats showed enhanced optomotor contrast sensitivity for low-spatial-frequency visual stimuli compared with wild-type-like baseline similarity.

Although the contrast sensitivities of the optomotor responses of transgenic rats were similar to those observed in the wild-type rats, they were enhanced for visual stimuli of low-spatial frequency after the degeneration of native photoreceptors.

After degeneration of native photoreceptors, transgenic rats showed enhanced optomotor contrast sensitivity for low-spatial-frequency visual stimuli compared with wild-type-like baseline similarity.

Although the contrast sensitivities of the optomotor responses of transgenic rats were similar to those observed in the wild-type rats, they were enhanced for visual stimuli of low-spatial frequency after the degeneration of native photoreceptors.

After degeneration of native photoreceptors, transgenic rats showed enhanced optomotor contrast sensitivity for low-spatial-frequency visual stimuli compared with wild-type-like baseline similarity.

Although the contrast sensitivities of the optomotor responses of transgenic rats were similar to those observed in the wild-type rats, they were enhanced for visual stimuli of low-spatial frequency after the degeneration of native photoreceptors.

After degeneration of native photoreceptors, transgenic rats showed enhanced optomotor contrast sensitivity for low-spatial-frequency visual stimuli compared with wild-type-like baseline similarity.

Although the contrast sensitivities of the optomotor responses of transgenic rats were similar to those observed in the wild-type rats, they were enhanced for visual stimuli of low-spatial frequency after the degeneration of native photoreceptors.

The results suggest that visual signals derived from ChR2-expressing retinal ganglion cells were reinterpreted by the brain to form behavior-related vision.

This result suggests that the visual signals derived from the ChR2-expressing RGCs were reinterpreted by the brain to form behavior-related vision.

The results suggest that visual signals derived from ChR2-expressing retinal ganglion cells were reinterpreted by the brain to form behavior-related vision.

This result suggests that the visual signals derived from the ChR2-expressing RGCs were reinterpreted by the brain to form behavior-related vision.

The results suggest that visual signals derived from ChR2-expressing retinal ganglion cells were reinterpreted by the brain to form behavior-related vision.

This result suggests that the visual signals derived from the ChR2-expressing RGCs were reinterpreted by the brain to form behavior-related vision.

The results suggest that visual signals derived from ChR2-expressing retinal ganglion cells were reinterpreted by the brain to form behavior-related vision.

This result suggests that the visual signals derived from the ChR2-expressing RGCs were reinterpreted by the brain to form behavior-related vision.

The results suggest that visual signals derived from ChR2-expressing retinal ganglion cells were reinterpreted by the brain to form behavior-related vision.

This result suggests that the visual signals derived from the ChR2-expressing RGCs were reinterpreted by the brain to form behavior-related vision.

The results suggest that visual signals derived from ChR2-expressing retinal ganglion cells were reinterpreted by the brain to form behavior-related vision.

This result suggests that the visual signals derived from the ChR2-expressing RGCs were reinterpreted by the brain to form behavior-related vision.

Channelrhodopsin-2 is described as a potentially useful optogenetic tool for restoring vision in photoreceptor degeneration.

Channelrhodopsin-2 (ChR2), one of the archea-type rhodopsins from green algae, is a potentially useful optogenetic tool for restoring vision in patients with photoreceptor degeneration, such as retinitis pigmentosa.

Channelrhodopsin-2 is described as a potentially useful optogenetic tool for restoring vision in photoreceptor degeneration.

Channelrhodopsin-2 (ChR2), one of the archea-type rhodopsins from green algae, is a potentially useful optogenetic tool for restoring vision in patients with photoreceptor degeneration, such as retinitis pigmentosa.

Channelrhodopsin-2 is described as a potentially useful optogenetic tool for restoring vision in photoreceptor degeneration.

Channelrhodopsin-2 (ChR2), one of the archea-type rhodopsins from green algae, is a potentially useful optogenetic tool for restoring vision in patients with photoreceptor degeneration, such as retinitis pigmentosa.

Channelrhodopsin-2 is described as a potentially useful optogenetic tool for restoring vision in photoreceptor degeneration.

Channelrhodopsin-2 (ChR2), one of the archea-type rhodopsins from green algae, is a potentially useful optogenetic tool for restoring vision in patients with photoreceptor degeneration, such as retinitis pigmentosa.

Channelrhodopsin-2 is described as a potentially useful optogenetic tool for restoring vision in photoreceptor degeneration.

Channelrhodopsin-2 (ChR2), one of the archea-type rhodopsins from green algae, is a potentially useful optogenetic tool for restoring vision in patients with photoreceptor degeneration, such as retinitis pigmentosa.

Channelrhodopsin-2 is described as a potentially useful optogenetic tool for restoring vision in photoreceptor degeneration.

Channelrhodopsin-2 (ChR2), one of the archea-type rhodopsins from green algae, is a potentially useful optogenetic tool for restoring vision in patients with photoreceptor degeneration, such as retinitis pigmentosa.

Cre-dependent recombination successfully enabled selective channelrhodopsin-2 expression in Sp5C projection neurons.

Source: A Viral Labelling Study of Spinal Trigeminal Nucleus Caudalis Projection Neurons Targeting the Parabrachial Nucleus.

Plant dependence on light and the absence of retinal were barriers to establishing plant optogenetics until recent progress overcame these difficulties.

For a long time, the dependence of plant growth on light and the absence of retinal, the rhodopsin chromophore, prevented the establishment of plant optogenetics until recent progress overcame these difficulties.

Source: Optogenetic Methods in Plant Biology

A combination of ElectroFluor 730p, X-Rhod-1, and ChR2 in mouse hearts enables simultaneous monitoring of transmembrane potential and cytosolic calcium while performing optogenetic manipulation with minimal crosstalk.

We here present a novel approach to simultaneously monitor transmembrane potential and cytosolic calcium, while also performing optogenetic manipulation. For this, we used the novel voltage-sensitive dye ElectroFluor 730p and the cytosolic calcium indicator X-Rhod-1 in mouse hearts expressing channelrhodopsin-2 (ChR2). By exploiting the isosbestic point of ElectroFluor 730p and avoiding the ChR2 activation spectrum, we here introduce a novel optical imaging and manipulation approach with minimal crosstalk.

Source: Recent advances and current limitations of available technology to optically manipulate and observe cardiac electrophysiology.

Light input can be switched on or off and tuned in intensity and duration to provide noninvasive, spatiotemporally resolved control of cellular processes.

Light can be turned on or off, and adjusting its intensity and duration allows optogenetic fine-tuning of cellular processes in a noninvasive and spatiotemporally resolved manner.

Source: Optogenetic Methods in Plant Biology

Optogenetic tools have been widely successful in multiple model organisms but have been used relatively rarely in plants.

optogenetic tools have been applied in a variety of model organisms with enormous success, but rarely in plants

Source: Optogenetic Methods in Plant Biology

Optogenetics uses natural or engineered photoreceptors in transgenic organisms to manipulate biological activities with light.

Optogenetics is a technique employing natural or genetically engineered photoreceptors in transgene organisms to manipulate biological activities with light.

Source: Optogenetic Methods in Plant Biology

Channelrhodopsin-2 is described as enabling millisecond neuromodulation.

Since the first demonstration of the millisecond neuromodulation ability of the channelrhodopsin-2 (ChR2)

Source: Applications and challenges of rhodopsin-based optogenetics in biomedicine

Optogenetic technology progressed rapidly in basic life science research, especially neurobiology, after the first demonstration of ChR2-based millisecond neuromodulation.

the application of optogenetic technology in basic life science research has been rapidly progressed, especially in neurobiology

Source: Applications and challenges of rhodopsin-based optogenetics in biomedicine

Channelrhodopsin-2-based optogenetic approaches can offer low-energy and localized control.

Source: Advances in Implantable Optogenetic Technology for Cardiovascular Research and Medicine

ChR2 expression in retinal ganglion cells of blind mice served as an early feasibility demonstration for optogenetic vision restoration.

Our first demonstration of the feasibility of such an approach involved expressing ChR2 in the retinal ganglion cells of blind mice

Source: Optogenetic Strategies for Vision Restoration

The paper reports ex vivo optogenetic pacing in ChR2 hearts.

Source: Wireless, battery-free, fully implantable multimodal and multisite pacemakers for applications in small animal models

In cardiac physiology, optogenetics has mainly used optically controlled depolarizing ion channels to control heart rate and for optogenetic defibrillation.

Source: Principles of Optogenetic Methods and Their Application to Cardiac Experimental Systems

ChR2-expressing cardiomyocytes show normal baseline and active excitable membrane and Ca2+ signaling properties and are sensitive even to approximately 1 ms light pulses.

Source: Principles of Optogenetic Methods and Their Application to Cardiac Experimental Systems

Expression of the chosen optogenetic tool in cardiac cells requires gene introduction by viral transduction or coupling via spark cells at the single-cell level, and transgenic expression or in vivo adenoviral delivery at system level.

Source: Principles of Optogenetic Methods and Their Application to Cardiac Experimental Systems

Named platforms aligned with the review's scope include LiGluR, LiGluN, LimGluR, optogating, ChR2, and Arch.

Primary papers for specific photoswitchable receptor platforms explicitly named in or strongly aligned with the review (LiGluR, LiGluN, LimGluR, optogating of P2X2)... Channelrhodopsin-2 (ChR2)... Arch.

Source: Optical control of neuronal ion channels and receptors

Comparison with the ChR2 C128T structure reveals a direct connection of the DC gate to the central gate and suggests that the gating mechanism is affected by subtle tuning of Schiff base interactions.

Comparison with the C128T structure reveals a direct connection of the DC gate to the central gate and suggests how the gating mechanism is affected by subtle tuning of the Schiff base's interactions.

Source: Structural insights into ion conduction by channelrhodopsin 2

In ChR2, the retinal Schiff base controls and synchronizes three gates that separate the cavities.

Central is the retinal Schiff base that controls and synchronizes three gates that separate the cavities.

Source: Structural insights into ion conduction by channelrhodopsin 2

The ChR2 structure reveals two intracellular cavities and two extracellular cavities connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

The structure reveals two cavities on the intracellular side and two cavities on the extracellular side. They are connected by extended hydrogen-bonding networks involving water molecules and side-chain residues.

Source: Structural insights into ion conduction by channelrhodopsin 2

The DC gate in ChR2 comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Separate from this network is the DC gate that comprises a water-mediated bond between C128 and D156 and interacts directly with the retinal Schiff base.

Source: Structural insights into ion conduction by channelrhodopsin 2

High-resolution structures were presented for ChR2 and the ChR2 C128T mutant.

We present high-resolution structures of ChR2 and the C128T mutant

Source: Structural insights into ion conduction by channelrhodopsin 2