Figure 3 Optogenetic manipulation of neuronal activity Figure 3 | Optogenetic manipulation of neuronal activity. Specialized light-sensitive ion channels or pumps genetically expressed in neurons can be activated by different wavelengths of light to cause membrane depolarization or hyperpolarization. When this process is induced in neuronal somata or dendrites, these effects regulate the rate at which action potentials are discharged (not shown). However, in this case, light is used to depolarize or hyperpolarize the axon terminals of the neuron and to stimulate or inhibit the release of neurotransmitters or neuropeptides, such as vasopressin. a | Channelrhodopsins (such as ChETA, illustrated here) are blue-light (∼470 nm)- sensitive ion channels that, when photoactivated, enable the influx of sodium ions into the axon terminals of the neuron, down their electrochemical gradient. The influx of positive ions depolarizes the terminals, thereby activating voltage-gated calcium channels and stimulating calcium-dependent release of neurotransmitters and neuropeptides. b | Archaerhodopsin T (ArchT) is a yellow-light (∼589 nm)-sensitive proton pump that, when photoactivated, moves positively charged ions from the intracellular compartment to the extracellular space, resulting in a net hyperpolarization of the axon terminals. In this example, photoactivation of ArchT hyperpolarizes the axon terminals and prevents the opening of voltage-gated calcium channels, thereby inhibiting the release of neurochemicals. Gizowski, C. & Bourque, C. W. (2017) The neural basis of homeostatic and anticipatory thirst Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.149