A V1-like receptor mediates vasopressin-induced flank marking behavior in hamster hypothalamus

Abstract

A vasopressin-sensitive mechanism within the medial preoptic area-anterior hypothalamus (MPOA-AH) appears to be essential for expression of a complex behavior involved in olfactory communication in Golden hamsters called flank marking. The present study investigated whether the induction of flank marking by arginine-vasopressin (AVP) within the MPOA-AH is mediated by a receptor that is more similar to the vasopressor (V1) or the antidiuretic (V2) AVP receptor. Adult male hamsters were anesthetized and implanted with a 26 gauge guide cannula stereotaxically aimed at the MPOA-AH and then microinjected with analogs of vasopressin, oxytocin, and selective V1 and V2 antagonists. Hamsters were tested for flank-marking behavior during a 5 or 10 min observation period following the injection of peptide in a vehicle of 100 nl of saline. None of the 15 analogs of AVP and oxytocin produced more flank marking than the 50.8 ± 16.2 and 76.8 ± 4.4 (mean ± SEM; n = 4) flank marks observed following injection of AVP at the 1 or 10 ng dose, respectively. The number of flank marks produced by each analog was found to be highly related to the pressor activity of that analog at both the 1 ng (ρ = +0.74, p < 0.01) and 10 ng (ρ= +0.82, p < 0.01) doses. In contrast, no statistically reliable relationship between flank marking and the antidiuretic activity of these analogs was found at either dose (1 ng: ρ = +0.07, p > 0.05; 10 ng;:ρ = +0.10, p > 0.05). In a second series of studies, microinjection of 2 different V1 antagonists into the MPOA-AH significantly (p < 0.005) inhibited flank marking in response to AVP. However, microinjection of a V2 antagonist or saline did not inhibit flank marking. These data indicate that the receptors mediating the induction of flank marking within the MPOA-AH are more similar to V1 (pressor) receptors than to V2 (antidiuretic) receptors.