Fig. 1

Effect of corticothalamic activation on thalamic cells is arousal dependent (a) Fluorescent micrograph from NTSR1-ChR mouse. Channelrhodopsin is expressed in somata (layer 6) and dendrites (layer 4-5a) of corticothalamic (CT) cells, as well as their axons in layer 4-5a, as well as in the thalamus. (b) Example ventral posterior thalamic response (tetrode recording) to a brief (2 ms, 4mW) light pulse to local CT axon terminals under urethane anesthesia. Cortex (S1) is not aligned topographically. (c) Typical responses (PSTHs) of thalamic units to brief (2 ms, 4mW) CT stimulation (insets: auto-correlograms). Thalamocortical (TC) cells either responded with brief excitatory peak followed by inhibition (top), or inhibition only (middle), and rebound, while thalamic reticular (nRT) units (bottom) usually showed excitation, followed inhibition. (d) Sleep/wake dependence of excitation/inhibition profile in a TC cell (rasterplot and normalized PSTH). Note the missing excitatory peak during wake state. (e) Ratio of units showing inhibition only is higher during wakefulness than during sleep. (f) In wake state, the excitatory peak is smaller (left), inhibition is longer (middle), and has a shorter onset (right) than during sleep. S1: primary somatosensory cortex; S2: secondary somatosensory cortex; VPM: ventral posteromedial nucleus of thalamus; VPL: ventral posterolateral nucleus of thalamus; Po: posterior nucleus, nRT: thalamic reticular nucleus.