Oxytocin and vasopressin in the medial amygdala differentially modulate approach and avoidance behavior toward illness-related social odor

Animals are known to recognize a specific odorant informing conspecific health condition, which plays a significant role in regulating their social communication. Here, we assess neural mechanisms regulating innate approach/avoidance response toward such conspecific odor cues in rats. Odor scent from healthy conspecifics induced approach behavior, while those from sick conspecifics produced avoidance response in odor-recipient male rats. Analysis of mRNA expression in several brain sites of odor recipient rats illustrated that induction of c-fos mRNA expression was found in the olfactory bulb (OB), the medial amygdala (MeA), the bed nucleus of stria terminalis (BnST), and the paraventricular nucleus of the hypothalamus (PVN), when exposed to conspecific odor. Moreover, in the MeA, expression of oxytocin (OT) receptor mRNA was increased when rats were exposed to healthy conspecific odor, while induction of arginine vasopressin (AVP) receptor 1a and 1b mRNA were found only when exposed to sick conspecific odor. Bilateral infusion of OT receptor (OTR) antagonist, (d(CH2)51,Tyr(Me)2,Thr4,Orn8,des-Gly-NH29)-Vasotocin, into the MeA blocked approach behavior to healthy odor, while those of AVP receptor antagonists, V1a selective: (Phenylac1,D-Tyr(Me)2,Arg6.8,Lys-NH29)-Vasopressin, and type 1 receptor antagonist: (Deamino-Pen1, Try(Me)2, Arg8)-Vasopressin, into the MeA inhibited avoidance response to sick odor. These findings provide evidence for an essential role of OT and AVP receptors, especially type 1a, in the MeA in regulating approach/avoidance behaviors, respectively, in social odorant communication.

Research Highlights▶Rats showed avoidance toward conspecific odors associated with illness state. ▶Approach behavior toward odor was regulated by oxytocin receptors in the medial amygdala. ▶Avoidance behavior toward sick odor was regulated by vasopressin 1a receptors in the medial amygdala.