Fig. 7: Increased D1-MSN excitability is necessary for stress-induced anhedonia and passive coping, and sufficient to promote negative affect in naïve mice. | Molecular Psychiatry

Fig. 7: Increased D1-MSN excitability is necessary for stress-induced anhedonia and passive coping, and sufficient to promote negative affect in naïve mice.

From: Cooperative synaptic and intrinsic plasticity in a disynaptic limbic circuit drive stress-induced anhedonia and passive coping in mice

Fig. 7

a Experimental timeline. b Representative image of AAV1-EF1α-DIO-eYFP and AAV1-EF1α-DIO-KIR2.1-2A-tdtomato expression in Dyn-Cre mice exposed to footshock stress. c Freezing to the training context and in response to fear-predictive cues on the day 4 test day. d Sucrose preference (n = 6; t-test; t(10) = 6.54, p < 0.0001) and (e) immobility in the FST across time (two-way ANOVA; treatment × time interaction; F(5, 70) = 2.701, p = 0.0273) in mice selectively expressing eYFP or KIR2.1 in D1-MSNs (f) experimental timeline. g Representative image of AAV9-EF1α-DIO-eYFP and AAV9-EF1α-DIO-KIRDN-2A-tdtomato expression in Dyn-Cre mice exposed to footshock stress. h Lack of generalized fear in mice expressing KIR DN in D1-MSNs. i Sucrose preference in naive mice selectively expressing eYFP or KIRDN in D1-MSNs (n = 9; t-test; t(16) = 2.53, p = 0.022). j Time spent immobile in naive mice selectively expressing eYFP or KIRDN in D1-MSNs (n = 9; t-test; t(16) = 2.707, p = 0.016).

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