Abstract
Region and cell-type restricted expression of light activated ion channels is the indispensable tool to study properties of synapses in specific circuits and to monitor synaptic alterations by various stimuli including neuromodulators and behaviors, both ex vivo and in vivo. These analyses require the light-activated proteins or viral vectors for their delivery that do not interfere with the phenomenon under study. Here, we report a case of such interference in which the high-level expression of Channelrhodopsin-2 (ChR2) introduced in the somatostatin-positive GABAergic neurons (SOM-INs) of the dorsomedial prefrontal cortex (dmPFC) by an adeno-associated virus vector (AAV) weakens the presynaptic GABAb receptor-mediated suppression of GABA release.
