Figure 4. Increasing reliability and recruitment of inhibition transforms corticothalamic function.
(A) Experimental setup: Optogenetic stimulation of VC neurons expressing Chronos-GFP while simultaneously recording in LGN and VC. AAV-Chronos-GFP was injected into VC at P0-1. (B) Representative images of Chronos-GFP expression in the VC and Chronos-GFP expressing corticothalamic axons in LGN at P6. Scale bars: 100, 100 and 10 µm. (C) Representative MUA rasters for 10 trials with LGN responses at each age. (D) Population mean post-stimulus time histogram of LGN spiking (n = 6 for each age group). At P6-11 VC optogenetic stimulation evokes purely excitatory responses in LGN, while in P13-14 animals initial excitation is followed by inhibition. (E) Population mean delay between LGN and VC spike onset (Kruskal-Wallis test, P6-7 vs P9-11 p=0.0020, P6-7 vs P13-14 p=0.0058, P9-11 vs P13-14 p=0.6247). (F) Population mean reliability: percentage of trials in which VC spike activity produced LGN spike activity (Kruskal-Wallis test, p=0.1744, 0.0057, 0.3960). (G) Population mean of spike-rate change in LGN following VC stimulation (1–100 ms after stim) (Wilcoxon signed-rank test vs baseline, P6-7: p=0.0313, P9-11: p=0.0313, P13-14: p=0.0313). (H) Population mean spike-rate change in LGN during inhibitory period (100–250 ms after stim). Significant inhibition is observed only at P13-14 (Wilcoxon signed-rank test vs baseline, P6-7: p=0.6563, P9-11: p=0.8438, P13-14: p=0.0313). (I) Cortical stimulation at spindle-burst frequencies (20 Hz) induces oscillations in LGN only at P9-11. VC stimulation at 20 Hz caused firing in LGN at all ages, but entrained LGN only at P9-11.