halorhodopsin

Post-illumination, the NpHR group showed improved contralateral forelimb akinesia compared with the pre-illumination state.

The results suggest that optogenetic modulation of reactive astrocytes alleviates astrocytic aberrant tonic inhibition of dopaminergic neurons and enhances degradation of α-Syn aggregates.

Optogenetic stimulation attenuates central post-stroke pain.

Optogenetic stimulation of NpHR expressed in reactive astrocytes in the SNpc of an A53T α-Syn overexpression PD rat model decreased α-Syn aggregates.

Optogenetic stimulation of NpHR expressed in reactive astrocytes in the SNpc of an A53T α-Syn overexpression PD rat model reduced GABA levels.

Channelrhodopsin, archaerhodopsin, and NpHR are examples of optogenetic tools applied in oral and craniofacial research for neural mechanism studies and in vivo oral behavioral test models.

The review covers use of channelrhodopsin, archaerhodopsin, and NpHR in studies of neural mechanisms and oral behavioral test models in vivo including orofacial movement, licking, eating, and drinking.

focusing on the ability to apply optogenetics to the study of basic scientific neural mechanisms and to establish different oral behavioral test models in vivo (orofacial movement, licking, eating, and drinking), such as channelrhodopsin (ChR), archaerhodopsin (Arch), and halorhodopsin from Natronomonas pharaonis (NpHR)

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Rhodopsin cyclases can be combined with cyclic nucleotide-gated channels in two-component optogenetics for depolarization or hyperpolarization of membrane potential.

We further show how they can be combined with cyclic nucleotide-gated channels in two-component optogenetics, for depolarization or hyperpolarization of membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Channelrhodopsins and their variants conduct cations or anions and are used for depolarization and hyperpolarization of membrane potential.

We address channelrhodopsins and variants thereof, which conduct cations or anions, for depolarization and hyperpolarization of the membrane potential.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Rhodopsin guanylyl cyclases and mutated variants with cyclic AMP specificity can regulate intracellular cGMP and cAMP levels.

Last, we report on a new addition to the optogenetic toolbox, which is rhodopsin guanylyl cyclases, as well as mutated variants with specificity for cyclic AMP. These can be used to regulate intracellular levels of cGMP and cAMP, which are important second messengers in sensory and other neurons.

Optogenetic inhibition of CeA CRF neurons reverses escalated alcohol drinking in alcohol-dependent rats.

The paper used the red-shifted inhibitory opsin Jaws to render donor photoreceptors light sensitive.

the paper transplanted optogenetically engineered photoreceptors, specifically cone-enriched donor populations rendered light sensitive with the red-shifted inhibitory opsin Jaws

Optogenetic inhibition of the CeA→BNST projection reverses escalated alcohol drinking and some withdrawal signs in dependent rats.

GCaMP imaging can be used for imaging individual cells in vitro and neural populations in vivo using fiber photometry.

The review highlights both benefits and caveats of optical approaches for acute brain slice studies and functional studies in vivo.

Optogenetics and GCaMP imaging have proven useful in dissecting functional circuitry within the brain and are likely to become essential investigative tools for deciphering neural networks controlling hormone secretion.

Optical imaging and optogenetics are transforming functional investigation of neuronal networks throughout the brain.

Natronomonas pharaonis halorhodopsin became an optogenetic neural silencer because it is the best-studied homologue, is facile to express and purify, and has advantageous properties.

Genetic mouse models combined with light-activated optical tools and GCaMP calcium imaging have been used to interrogate neural circuitry controlling hormone secretion.

Optogenetic tools are well suited to treat retinas with photoreceptor degeneration independently of the underlying mutation.

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

Genetically modified viral vectors broaden the ability to express genes of interest and support inducible manipulations in neural systems.

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Engineered G protein-coupled receptors activated by otherwise inert drug-like small molecules provide a chemogenetic or pharmacogenetic approach for selective remote control of neuronal activity.

Recent advance in genetics has also allowed development of novel pharmacological tools to selectively and remotely control neuronal activity using engineered G protein-coupled receptors, which can be activated by otherwise inert drug-like small molecules such as the designer receptors exclusively activated by designer drug, a form of chemogenetics.

Engineered G protein-coupled receptors activated by otherwise inert drug-like small molecules provide a chemogenetic or pharmacogenetic approach for selective remote control of neuronal activity.

Recent advance in genetics has also allowed development of novel pharmacological tools to selectively and remotely control neuronal activity using engineered G protein-coupled receptors, which can be activated by otherwise inert drug-like small molecules such as the designer receptors exclusively activated by designer drug, a form of chemogenetics.

Engineered G protein-coupled receptors activated by otherwise inert drug-like small molecules provide a chemogenetic or pharmacogenetic approach for selective remote control of neuronal activity.

Recent advance in genetics has also allowed development of novel pharmacological tools to selectively and remotely control neuronal activity using engineered G protein-coupled receptors, which can be activated by otherwise inert drug-like small molecules such as the designer receptors exclusively activated by designer drug, a form of chemogenetics.

Engineered G protein-coupled receptors activated by otherwise inert drug-like small molecules provide a chemogenetic or pharmacogenetic approach for selective remote control of neuronal activity.

Recent advance in genetics has also allowed development of novel pharmacological tools to selectively and remotely control neuronal activity using engineered G protein-coupled receptors, which can be activated by otherwise inert drug-like small molecules such as the designer receptors exclusively activated by designer drug, a form of chemogenetics.

Engineered G protein-coupled receptors activated by otherwise inert drug-like small molecules provide a chemogenetic or pharmacogenetic approach for selective remote control of neuronal activity.

Recent advance in genetics has also allowed development of novel pharmacological tools to selectively and remotely control neuronal activity using engineered G protein-coupled receptors, which can be activated by otherwise inert drug-like small molecules such as the designer receptors exclusively activated by designer drug, a form of chemogenetics.

Engineered G protein-coupled receptors activated by otherwise inert drug-like small molecules provide a chemogenetic or pharmacogenetic approach for selective remote control of neuronal activity.

Recent advance in genetics has also allowed development of novel pharmacological tools to selectively and remotely control neuronal activity using engineered G protein-coupled receptors, which can be activated by otherwise inert drug-like small molecules such as the designer receptors exclusively activated by designer drug, a form of chemogenetics.

Engineered G protein-coupled receptors activated by otherwise inert drug-like small molecules provide a chemogenetic or pharmacogenetic approach for selective remote control of neuronal activity.

Recent advance in genetics has also allowed development of novel pharmacological tools to selectively and remotely control neuronal activity using engineered G protein-coupled receptors, which can be activated by otherwise inert drug-like small molecules such as the designer receptors exclusively activated by designer drug, a form of chemogenetics.

Chemogenetics can be activated via a systemic drug without indwelling fiber optics and acts in a more naturalistic modulatory fashion through second-messenger pathways than optogenetics.

Optogenetic and chemogenetic approaches allow mechanistic, temporally specific, cell-type-specific, and circuit-specific neural regulation of behaviors.

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

eNpHR is a chloride pump that mediates light-activated hyperpolarization.

Ectopic expression of channelrhodopsin or eNpHR can make inactive photoreceptors or other intact retinal cells sensitive to light, thereby restoring the basic retinal function of light perception.

DREADD technology is presented as the most robust model of chemogenetics.

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.

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.

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.

Halorhodopsin is an archaeal light-driven Cl- pump.

Krokinobacter eikastus rhodopsin 2 is a light-driven Na+ pump.

BR, HR, PR, FR, and KR2 are classified as DTD, TSA, DTE, NTQ, and NDQ rhodopsins, respectively.

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.

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.

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

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.

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.

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.

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.

ArchT is presented as an improved archaerhodopsin-family silencer with improved light sensitivity relative to Arch.

Mac is presented as a blue-green light-driven proton pump relevant for multicolor silencing.

Using optogenetics to control network excitability and associated brain diseases involves challenges and pitfalls.

We also point out some of the challenges and pitfalls in relation to possible outcomes of using optogenetics for controlling network excitability, and associated brain diseases.

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

Halorhodopsins are described as light-driven inward chloride pumps used as inhibitory neural silencing tools.

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 review discusses expression, trafficking, spectra, kinetics, and engineering as relevant properties of inhibitory optogenetic silencing tools.

This review centers on inhibitory microbial opsins used for light-driven silencing of targeted neurons.

This review summarizes molecular optogenetic tools for perturbing distinct cell types, projections, and intracellular biochemical signaling.

PubMed/PMC confirm the review focuses on molecular optogenetic tools for perturbing distinct cell types, projections, and intracellular biochemical signaling

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.

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.

The review explicitly discusses microbial opsins, including channelrhodopsins, halorhodopsins, and bacteriorhodopsins/archaerhodopsins, as core optogenetic tool classes.

explicitly discusses microbial opsins (including channelrhodopsins, halorhodopsins, bacteriorhodopsins/archaerhodopsins) ... as core tool classes

The review explicitly discusses OptoXRs as a core optogenetic tool class for intracellular signaling control.

explicitly discusses ... OptoXRs as core tool classes

Inhibitory halorhodopsin NpHR expressed in hippocampal principal cells has been used to effectively control chemically and electrically induced epileptiform activity in slice preparations.

Expression of the inhibitory halorhodopsin NpHR in hippocampal principal cells has been recently used as a tool to effectively control chemically and electrically induced epileptiform activity in slice preparations

Inhibitory halorhodopsin NpHR has been used to reduce in vivo spiking induced by tetanus toxin injection in the motor cortex.

and to reduce in vivo spiking induced by tetanus toxin injection in the motor cortex.

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 paper engineers NpHR by adding an N-terminal signal peptide and a C-terminal ER export sequence to create eNpHR.

The paper engineers NpHR to reduce ER retention/aggregation by adding an N-terminal signal peptide and a C-terminal ER export sequence, yielding enhanced NpHR (eNpHR).

eNpHR is an enhanced Natronomonas halorhodopsin engineered for optogenetic applications.

eNpHR: a Natronomonas halorhodopsin enhanced for optogenetic applications

eNpHR has improved membrane localization and larger photocurrents relative to the parent NpHR construct.

yielding enhanced NpHR (eNpHR) with improved membrane localization and larger photocurrents

Post-illumination, the NpHR group showed improved contralateral forelimb akinesia compared with the pre-illumination state.

Source: Optogenetic regulation of chloride ions in reactive astrocytes may mitigate Parkinson's disease pathology.

The results suggest that optogenetic modulation of reactive astrocytes alleviates astrocytic aberrant tonic inhibition of dopaminergic neurons and enhances degradation of α-Syn aggregates.

Source: Optogenetic regulation of chloride ions in reactive astrocytes may mitigate Parkinson's disease pathology.

Optogenetic stimulation attenuates central post-stroke pain.

Source: Optogenetic stimulation attenuates central post-stroke pain via BDNF/TrkB signaling pathway modulation in the ascending pain modulation system.

Optogenetic stimulation of NpHR expressed in reactive astrocytes in the SNpc of an A53T α-Syn overexpression PD rat model decreased α-Syn aggregates.

Source: Optogenetic regulation of chloride ions in reactive astrocytes may mitigate Parkinson's disease pathology.

Optogenetic stimulation of NpHR expressed in reactive astrocytes in the SNpc of an A53T α-Syn overexpression PD rat model reduced GABA levels.

Source: Optogenetic regulation of chloride ions in reactive astrocytes may mitigate Parkinson's disease pathology.

Channelrhodopsin, archaerhodopsin, and NpHR are examples of optogenetic tools applied in oral and craniofacial research for neural mechanism studies and in vivo oral behavioral test models.

Source: Optogenetics in oral and craniofacial research

The review covers use of channelrhodopsin, archaerhodopsin, and NpHR in studies of neural mechanisms and oral behavioral test models in vivo including orofacial movement, licking, eating, and drinking.

focusing on the ability to apply optogenetics to the study of basic scientific neural mechanisms and to establish different oral behavioral test models in vivo (orofacial movement, licking, eating, and drinking), such as channelrhodopsin (ChR), archaerhodopsin (Arch), and halorhodopsin from Natronomonas pharaonis (NpHR)

Source: Optogenetics in oral and craniofacial research

The review highlights both benefits and caveats of optical approaches for acute brain slice studies and functional studies in vivo.

Source: Optical Approaches for Interrogating Neural Circuits Controlling Hormone Secretion

Optogenetics and GCaMP imaging have proven useful in dissecting functional circuitry within the brain and are likely to become essential investigative tools for deciphering neural networks controlling hormone secretion.

Source: Optical Approaches for Interrogating Neural Circuits Controlling Hormone Secretion

Optical imaging and optogenetics are transforming functional investigation of neuronal networks throughout the brain.

Source: Optical Approaches for Interrogating Neural Circuits Controlling Hormone Secretion

Natronomonas pharaonis halorhodopsin became an optogenetic neural silencer because it is the best-studied homologue, is facile to express and purify, and has advantageous properties.

Source: Microbial Halorhodopsins: Light-Driven Chloride Pumps

Genetic mouse models combined with light-activated optical tools and GCaMP calcium imaging have been used to interrogate neural circuitry controlling hormone secretion.

Source: Optical Approaches for Interrogating Neural Circuits Controlling Hormone Secretion

These optogenetic and chemogenetic toolboxes have enabled advances in deciphering nervous system function and its influence on physiological processes in health and disease.

These novel toolboxes are enabling significant advances in deciphering how the nervous system works and its influence on various physiological processes in health and disease.

Source: Optogenetics and pharmacogenetics: principles and applications

Bioengineered light-sensitive ion channels including channelrhodopsins, halorhodopsin, and archaerhodopsins enable light-based artificial modulation of neuronal activity in optogenetics.

Identification and subsequent bioengineering of light-sensitive ion channels (e.g., channelrhodopsins, halorhodopsin, and archaerhodopsins) from the bacteria have made it possible to use light to artificially modulate neuronal activity, namely optogenetics.

Source: Optogenetics and pharmacogenetics: principles and applications

Optogenetics and pharmacogenetics allow selective and bidirectional modulation of defined neuronal populations with unprecedented specificity.

The cutting-edge optogenetics and pharmacogenetics are powerful tools in neuroscience that allow selective and bidirectional modulation of the activity of defined populations of neurons with unprecedented specificity.

Source: Optogenetics and pharmacogenetics: principles and applications

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.

Source: Biophysical Properties of Optogenetic Tools and Their Application for Vision Restoration Approaches

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.

Source: Optogenetic Approaches for Controlling Seizure Activity

Halorhodopsin is an archaeal light-driven Cl- pump.

Source: Ion-pumping microbial rhodopsins

BR, HR, PR, FR, and KR2 are classified as DTD, TSA, DTE, NTQ, and NDQ rhodopsins, respectively.

Source: Ion-pumping microbial rhodopsins

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.

Source: <scp>WONOEP</scp> appraisal: Optogenetic tools to suppress seizures and explore the mechanisms of epileptogenesis