Figure 1.

24 Hours of Social Isolation Induces Synaptic Potentiation onto DRN DA Neurons

(A) AMPAR/NMDAR ratios recorded from VTA DA neurons in mice socially isolated for 24 hr (n = 12) were not significantly different from group-housed mice (n = 8; unpaired t test: t₁₈ = 0.73, p = 0.47).

(B) Low- (upper panel) and high-magnification (lower panels) confocal images of the DRN from a TH-GFP mouse showing GFP-expressing (green) and post hoc immunohistochemically verified TH-expressing (red) DA neurons with white arrows indicating co-labeled neurons.

(C) AMPAR/NMDAR ratios recorded from DRN DA neurons in mice socially isolated for 24 hr, either in a familiar cage or a novel cage (familiar isolated or novel isolated, respectively), were significantly greater than group-housed mice in familiar or novel cages (one-way ANOVA: F_3,47 = 5.910, ^∗∗p = 0.0017; Newman-Keuls post hoc tests: ^∗p < 0.05, ^∗∗p < 0.01; n = 19 naive, 17 familiar isolated, 9 novel grouped, and 6 novel isolated). Scale bars, 20 pA, 20 ms.

(D) The AMPAR rectification index in DRN DA neurons was significantly greater in socially isolated mice, relative to naive mice (unpaired t test: t₂₁ = 2.417, ^∗p = 0.0248, n = 9 naive, 14 isolated).

(E) Normalized AMPAR-mediated EPSC amplitude during bath application of NASPM, and representative averaged EPSCs from a naive and socially isolated mouse (inset shows % change in EPSC amplitude following NASPM, relative to baseline). NASPM significantly reduced EPSC amplitude in socially isolated mice (n = 7), relative to naive mice (n = 8; unpaired t test: t₁₃ = 2.853, ^∗p = 0.0136). Scale bars, 10 pA, 10 ms.

(F) Proposed model of AMPARs at synapses onto DRN DA neurons in group-housed mice and following social isolation.

Data are represented as mean ± SEM. See also Figure S1.