Skip to main content
. Author manuscript; available in PMC: 2016 Apr 29.
Published in final edited form as: Nature. 2015 Oct 21;526(7575):705–709. doi: 10.1038/nature15398

Figure 3. PFC-dependent visTRN modulation suggests PFC-TRN functional coupling is required for visual gain control.

Figure 3

(a) Intersectional tagging of visTRN based on connectivity and genetic identity. Inset: Maximum projection of ten 1μm confocal images. Cells were labeled with ChR2-EYFP and stained with anti-GFP. (b) Raster of two visTRN neurons triggered on task initiation. Note the reduction of firing rate between the first trigger (trial initiation) and second one (stimulus presentation) during the ‘attend to vision’ condition, but the opposite during ‘attend to audition’ condition. Fading gray boxes denote the jitter of the anticipatory period. (c) Group analysis of b, showing a scatter plot of 138 visTRN neurons (n = 4 animals, p < 0.005, Wilcoxon rank-sum test performed over all cells). Orange crosshair indicates mean ± 95% confidence interval. (d) PFC activity was disrupted during stimulus anticipation to examine impact on visTRN activity. (e) PFC disruption diminished visTRN attentional modulation. (f–g) Behavioral performance is causally dependent on visTRN attentional modulation. (f) Optogenetic activation of retrogradely tagged visTRN neurons resulted in preferential diminishing of visual trials (mean ± s.e.m., n = 12 sessions from 3 mice, * p < 0.05, ** p < 0.01, *** p < 0.001, Wilcoxon rank-sum Test), consistent with this manipulation lowering visual gain. (g) In contrast, optogenetic inhibition of visTRN preferentially diminished auditory trials, consistent with inappropriate visual gain increase (n = 12 sessions from 3 mice).