Fig. 6: 5-HTDR→VTA neurons bidirectionally modulate stress susceptibility.
From: A discrete serotonergic circuit regulates vulnerability to social stress
a, e Experimental timeline and optogenetic stimulation protocol. b, f Quantitative data showing no difference in social interaction time or social interaction ratio between the resilient-eNpHR group and the mCherry group (b, eNpHR, n = 9 mice; mCherry, n = 8 mice; one-way ANOVA, interaction: F1,15 = 0.594, P = 0.453, SI ratio: F1,15 = 0.407, P = 0.533) or between the susceptible-channelrhodopsin-2 (sus-ChR2) group and the susceptible-enhanced yellow fluorescent protein (sus-eYFP) group (f, eYFP, n = 9 mice; ChR2, n = 8 mice; one-way ANOVA, interaction: F1,15 = 0.241, P = 0.63, SI ratio: F1,15 = 2.62, P = 0.126). c, d One week of the inhibition of 5-HTDR→VTA neurons in resilient mice counteracted this phenotype to induce a susceptible-like phenotype (d, eNpHR, n = 8 mice; mCherry, n = 7 mice; one-way ANOVA, interaction: F1,13 = 10.613, P = 0.006, SI ratio: F1,13 = 5.546, P = 0.035), whereas acute stimulation during the social interaction test had no effect; (c, eNpHR, n = 8 mice; mCherry, n = 8 mice; one-way ANOVA, interaction: F1,14 = 0.95, P = 0.346, SI ratio: F1,14 = 2.231, P = 0.157). g, h The time spent in the interaction zone with the target of ChR2-stimulated susceptible mice was significantly increased during the acute (g, eYFP, n = 8 mice; ChR2, n = 8 mice; one-way ANOVA, interaction: F1,14 = 9.497, P = 0.008, SI ratio: F1,14 = 7.375, P = 0.017) or chronic stimulation of 5-HTDR→VTA neurons (h, eYFP, n = 6 mice; ChR2, n = 8 mice; one-way ANOVA, interaction: F1,12 = 4.773, P = 0.049, SI ratio: F1,12 = 5.989, P = 0.031). Data are represented as mean ± SEM. NS: not statistically significant. *P < 0.05, **P < 0.01. Source data are provided as a Source Data file.
