Figure 2.

Single-point channelrhodopsin-2 (ChR2) cortical stimulation and electroencephalography (EEG) and electromyography (EMG) recording reveal rapid response recovery after reperfusion despite persistent deficits in forepaw stimulation-evoked cortical EEG responses. Channelrhodopsin-2 and sensory stimulation are interleaved and repeated every 10 seconds. (A) Representative traces of forepaw stimulation-evoked EEG (left column), ChR2 stimulation-evoked EEG (middle column), and ChR2-stimulation-evoked EMG (right column). (B) Changes of direct current-EEG (n=5), 0.3 to 3 Hz EEG power (n=5), ChR2-evoked peak amplitude (n=5), ChR2-evoked EMG responses integration (n=5), and forepaw-evoked peak amplitude (n=5) are shown from top to bottom. Except for DC-EEG, the other statistical data were based on relative values, which were normalized to pre-common carotid artery occlusion (CCAO) value as 100%. The shaded band indicates s.e.m. These findings are consistent with previous work¹ and use different methods of anesthesia (ketamine/xylazine in the present experiment versus urethane in the previous one) and cortical temperature regulation (∼36.5°C). (C) Statistical analysis of ChR2-mediated EEG (ChR2-EEG) and EMG (ChR2-EMG) responses, and forepaw stimulation-mediated EEG responses (forepaw-EEG) after 5 minute CCAO and reperfusion at select time points (*P<0.05, **P<0.01, ChR2-EEG versus ChR2-EMG; ^$P<0.05, ChR2-EMG versus forepaw-EEG; ^#P<0.05, ^##P<0.01, ChR2-EEG versus forepaw-EEG, Student's t-test). All data are shown as mean±s.e.m.