Social interactions are essential for human health and society. However, the neural circuitry basis for many socialbehaviorsremainsuncertain.Besideclassicalbehaviorssuchasaggression,pairbondingandparenting, recentresearchhasdemonstratedthatrodentsarealsocapableofbehaviorstocomfortdistressedindividuals. Tostudytheneuralbasisoftheseprosocialbehaviors,werecentlyadaptedaprotocolthatproducesconsolation- like behavior in socially monogamous prairie voles to the widely used C57BL/6J mice. Our preliminary experiments indicate an important role for the paraventricular nucleus of the thalamus (PVT) in controlling consolation-likebehaviorinmice.Comfortingadistressedcagemateelicitedrobustc-FosexpressioninthePVT and pharmacogenetic silencing of the PVT dramatically reduced consolation-like behavior. Based on these intriguingresults,weproposeto(Aim1)performinvivoelectrophysiologyrecordingandoptogeneticmanipulation ofPVTtodeterminetheroleofPVTduringconsolation-likebehavior.Incomfortingmice,therewasalsostrong activationoftheprefrontalcortexandventralsubiculumwhicharemajorinputstothePVT.Wethereforepropose to(Aim2)identifytheinputsresponsibleforPVTactivityduringprosocialbehaviorandexpandourunderstanding of the circuitry using viral tracing. The proposed studies defining the prosocial neural circuitry will add to the knowledgebasenecessaryfortreatingconditionswithsocialdeficits.
Helping others when they are distressed is one of the most noble behaviors, but its underlying neural mechanisms are largely unknown. We propose to examine the neural circuitry underlying helping or prosocial behavior by dissecting our new mouse model of consolation-like behavior with viral, optogenetic, as well as in vivo recording and imaging tools. Ultimately, understanding the neural circuits governing prosocial behaviors should help diagnose and treat conditions with social deficits.
