(A) Infusion of D1 receptor (D1R) antagonist SCH23390 into NAc prior to VTA stimulation during social interaction. (B) Compared to control saline infusion, D1R antagonism attenuated light-evoked increases in social behavior (n=15, LME model, t18=2.29, p=0.035). (C) Opto-D1 design: replacing intracellular loops of rhodopsin with those of D1R. (D) In vitro GPCR signaling assays show selective upregulation of cAMP but not IP3 or cGMP pathways by Opto-D1 (n=3 samples, 4 readings each, unpaired t-test, p=0.002). (E) Infusion of DIO-Opto-D1 virus into NAc of Drd1::Cre mice for selective expression in D1R+ NAc cells. (F) Illumination of Opto-D1 in NAc D1 cells with continuous 473 nm light increased social interaction compared to eYFP controls (n=10 per group, LME model, t18=2.64, p=0.018). (G) Example recording of NAc activity with Opto-D1 activation. (H) PSTH: light-evoked increase in NAc firing with Opto-D1. (I) Summary graph from (H): increase in NAc firing during activation of Opto-D1 (Wilcoxon signed-rank test, p=0.01). (J) Infusion of DIO-ChR2 into NAc of Drd1::Cre mice. (K) Tonic 10 Hz stimulation of NAc D1R cells increased social interaction (n=6, LME model, t11=2.26, p=0.039). See also Figure S5.