channelrhodopsins

Channelrhodopsins from green algae enabled precise light-controlled manipulation of neuronal activity and are described as having revolutionized neuroscience.

Channelrhodopsins from green algae, for example, have revolutionized neuroscience by enabling precise, light-controlled manipulation of neuronal activity.

Channelrhodopsins from green algae have revolutionized neuroscience by enabling precise, light-controlled manipulation of neuronal activity.

Optogenetic techniques have been applied to partially restore vision in blind patients and are being explored for neurological, psychiatric, cardiac, and immunological disorders.

Microbial channelrhodopsins allow precise manipulation of neuronal and cardiac activities.

Vertebrate rhodopsins can modulate ion channels through GPCR pathways.

Optogenetics provides precise spatiotemporal control, minimal invasiveness, and tunable reversibility for controlling protein activity and cellular processes.

The review covers genetically encoded light-sensitive ion channel actuators and modulators with diverse ion selectivity and spectral sensitivity.

Animals expressing channelrhodopsin in specific neuronal populations have been used to map neural circuitry and examine post junctional neural effects on GI motility.

GCaMP-expressing animals have been used to characterize Ca2+ signalling behaviours of distinct classes of interstitial cells of Cajal and smooth muscle cells throughout the GI musculature.

Mice expressing GCaMP or RCaMP allow cell-specific visualization of Ca2+ signalling behaviours in the gastrointestinal tract.

Mice expressing channelrhodopsins or halorhodopsins allow light-based manipulation of specific signalling pathways.

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.

The review covers engineering and applications of upconversion optogenetic systems that incorporate multiple emissive UCNPs into various light-gated channelrhodopsin or ligand systems, and discusses technical improvements for more precise and efficient membrane-channel control.

Established optogenetic tools such as channelrhodopsins are mainly stimulated by UV or visible light, which raises concerns about photodamage, limited tissue penetration, and invasive optical fiber implantation.

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.

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.

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.

High-resolution structural data and molecular dynamics calculations support models that explain channelrhodopsin activation and ion conductance through chromophore isomerization, structural changes, proton transfer reactions, and water rearrangement across timescales from femtoseconds to minutes.

With significant support from a high-resolution 3D structure and from molecular dynamics calculations, scientists are now able to develop models that conclusively explain ChR activation and ion conductance on the basis of chromophore isomerization, structural changes, proton transfer reactions, and water rearrangement on timescales ranging from femtoseconds to minutes.

Channelrhodopsins are versatile neuroscience tools for light-induced activation of selected cells or cell types with high temporal and spatial precision.

In neuroscience, ChRs constitute the most versatile tools for the light-induced activation of selected cells or cell types with unprecedented precision in time and space.

Many channelrhodopsin variants have been discovered or engineered.

In recent years, many ChR variants have been discovered or engineered

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

OptoXRs are rhodopsin-GPCR chimeras for controlling intracellular signaling cascades.

Channelrhodopsins, halorhodopsins, bacteriorhodopsins, and OptoXRs are explicitly named tool classes associated with the paper's scope.

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.

Optogenetics as described here is based on channelrhodopsins that are genetically integrated into neuronal membranes and activated by brief light pulses delivered through an optical fibre.

This technique is based on a group of light-sensitive ion channels called channelrhodopsins that can be integrated by genetic engineering into the neuronal cell membrane. By a laser-diode-coupled optical fibre targeting a specific neuronal population of interest, a brief light pulse can then activate those neurones.

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.

Activation of light sensitive channels was used in the authors' recent work to restore respiratory function after experimental spinal cord injury.

we briefly review the history of various attempts to restore breathing after C2 hemisection, and focus on our recent work using the activation of light sensitive channels to restore respiratory function after experimental SCI.

Light-induced activity can be used to investigate the central nervous system respiratory circuitry that controls diaphragmatic function.

We also discuss how such light-induced activity can help shed light on the inner workings of the central nervous system respiratory circuitry that controls diaphragmatic function.

Expression of channelrhodopsins is presented as a therapeutically relevant alternative approach for restoring respiratory function after spinal cord injury.

With the emergence of new and powerful tools from molecular neuroscience, new therapeutically relevant alternatives to these approaches have become available, including expression of light sensitive proteins called channelrhodopsins.

Channelrhodopsins from green algae enabled precise light-controlled manipulation of neuronal activity and are described as having revolutionized neuroscience.

Channelrhodopsins from green algae, for example, have revolutionized neuroscience by enabling precise, light-controlled manipulation of neuronal activity.

Source: Sensing a rainbow of colors: algal photoreceptors

Channelrhodopsins from green algae have revolutionized neuroscience by enabling precise, light-controlled manipulation of neuronal activity.

Source: Sensing a rainbow of colors: algal photoreceptors

Microbial channelrhodopsins allow precise manipulation of neuronal and cardiac activities.

Source: Optogenetic engineering for ion channel modulation

Animals expressing channelrhodopsin in specific neuronal populations have been used to map neural circuitry and examine post junctional neural effects on GI motility.

Source: Insights on gastrointestinal motility through the use of optogenetic sensors and actuators.

Mice expressing channelrhodopsins or halorhodopsins allow light-based manipulation of specific signalling pathways.

Source: Insights on gastrointestinal motility through the use of optogenetic sensors and actuators.

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.

Source: Microbial Rhodopsin Optogenetic Tools: Application for Analyses of Synaptic Transmission and of Neuronal Network Activity in Behavior

The review covers engineering and applications of upconversion optogenetic systems that incorporate multiple emissive UCNPs into various light-gated channelrhodopsin or ligand systems, and discusses technical improvements for more precise and efficient membrane-channel control.

Source: Near‐Infrared Manipulation of Membrane Ion Channels via Upconversion Optogenetics

Established optogenetic tools such as channelrhodopsins are mainly stimulated by UV or visible light, which raises concerns about photodamage, limited tissue penetration, and invasive optical fiber implantation.

Source: Near‐Infrared Manipulation of Membrane Ion Channels via Upconversion Optogenetics

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

High-resolution structural data and molecular dynamics calculations support models that explain channelrhodopsin activation and ion conductance through chromophore isomerization, structural changes, proton transfer reactions, and water rearrangement across timescales from femtoseconds to minutes.

With significant support from a high-resolution 3D structure and from molecular dynamics calculations, scientists are now able to develop models that conclusively explain ChR activation and ion conductance on the basis of chromophore isomerization, structural changes, proton transfer reactions, and water rearrangement on timescales ranging from femtoseconds to minutes.

Source: Biophysics of Channelrhodopsin

Channelrhodopsins are versatile neuroscience tools for light-induced activation of selected cells or cell types with high temporal and spatial precision.

In neuroscience, ChRs constitute the most versatile tools for the light-induced activation of selected cells or cell types with unprecedented precision in time and space.

Source: Biophysics of Channelrhodopsin

Many channelrhodopsin variants have been discovered or engineered.

In recent years, many ChR variants have been discovered or engineered

Source: Biophysics of Channelrhodopsin

Optogenetic reagents including proteins and photochemical switches were used to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis.

we used optogenetic reagents, both proteins and photochemical switches, to vary steady-state bioelectrical properties of non-spiking embryonic cells in Xenopus laevis

Source: Optogenetics in Developmental Biology: using light to control ion flux-dependent signals in Xenopus embryos

Experiments on the dark phenotype yielded evidence that ion flux direction via common optogenetic reagents may be reversed or unpredictable in non-neural cells.

Experiments on this "dark phenotype" yielded evidence that the direction of ion flux via common optogenetic reagents may be reversed, or unpredictable in non-neural cells

Source: Optogenetics in Developmental Biology: using light to control ion flux-dependent signals in Xenopus embryos

The majority of tested reagents also induced phenotypes in dark-kept controls.

however, the majority of reagents also induced phenotypes in controls kept in the dark

Source: Optogenetics in Developmental Biology: using light to control ion flux-dependent signals in Xenopus embryos

The majority of tested reagents caused a significant increase in the percentage of light-exposed tadpoles showing phenotypes associated with altered membrane voltage.

The majority of reagents we tested caused a significant increase in the percentage of light-exposed tadpoles showing relevant phenotypes

Source: Optogenetics in Developmental Biology: using light to control ion flux-dependent signals in Xenopus embryos

When used with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems.

When used in combination with rigorous controls, optogenetics can be a powerful tool for investigating ion-flux based signaling in non-excitable systems

Source: Optogenetics in Developmental Biology: using light to control ion flux-dependent signals in Xenopus embryos

Channelrhodopsins, halorhodopsins, bacteriorhodopsins, and OptoXRs are explicitly named tool classes associated with the paper's scope.

Source: Molecular Tools and Approaches for Optogenetics