(A–C) Extracellular recording showing complete optogenetic silencing of the visual cortex. Shown are a deep-layer neuron’s peri-stimulus timing histogram (PSTH) of spiking response to grating at the preferred direction in the absence (A) or presence (B) of LED illumination. Blue bar indicates LED illumination, and the gray shadow indicates period of visual stimulation. (C) Summary plot of spike rate before, during and after LED activation (same data as Figure 2B ). Note that the spike rate was calculated by averaging across all 12 directions of the drifting gratings, many of which did not evoke responses due to the neurons’ selectivity. LED activation was able to silence all the recorded neurons at all directions (p = 0.0007, paired t-test between No LED and LED; and p = 0.0003, paired t-test between LED and recovery, n = 8). Extracellular recording showing layer 4 neurons do not receive callosal inputs. Shown are a layer 4 neuron’s PSTHs to grating at the preferred direction in the absence (D) or presence (E) of LED illumination of the visual cortex in other hemisphere. (F) Summary plot of spike rate before and during LED activation. No change of visually evoked spiking response was seen (p = 0.37, paired t-test, n = 9). (G–J) Field potential recording showing optogenetic silencing of the visual cortex does not affect thalamocortical transmission by activating GABAB receptors. (G) Example traces of visually evoked potential (VEP) in control (red), with GABAB receptor agonist Baclofen (10 μM, Tocris, solid blue), and with Baclofen + CGP54626, a GABAB receptor antagonist (10 μM, Tocris, dashed blue). (H) Summary plots of VEP amplitudes. The decrease of VEP amplitude by Baclofen was reversed by CGP (p = 0.002, paired t-test, n = 4). (I) Example traces of VEP in control (red), with LED illumination (solid blue), and with LED and 15 – 45 min after (dashed blue) CGP54626 application. (J) Summary plots of VEP amplitudes. No difference is seen between LED and LED+CGP conditions (p = 0.73, paired t-test, n = 6).