Effects of Gonadal Steroids on the Mesoctocin and Vasotocin Systems in the Brain of the Domestic Hen.

The nonapeptides oxytocin and vasopressin and their avian homologues mesotocin and vasotocin form part of the neural systems that govern social behaviour. Neurones in the paraventricular nucleus (PVN) and bed nucleus of the stria terminalis (BnST) are sensitive to environmental and hormonal changes. Gonadal steroids can influence oxytocin and vasopressin in mammals; we sought to investigate how changes in gonadal steroids affect the mesotocin and vasotocin systems of juvenile (38-day-old) female chickens. Specifically we compared mesotocin and vasotocin mRNA expression using in situ hybridization, mesotocin protein using immunohistochemistry and mesotocin receptor binding using autoradiography 24 hours following a single i.m. injection of either testosterone (20mg/ml/kg bw), oestradiol (10mg/ml/kg bw), progesterone (20mg/ml/kg bw) or corn oil control (1ml/kg bw); n=5-9 per group) administered following priming with diethylstilsbetrol (1g initial and 0.5g secondary priming i.m., 10g/ml in corn oil). Brains were collected, frozen on dry ice and sectioned at 15µm until processing. Animal care and use protocols were carried out under the UK Home Office licence guidelines [Animal Scientific Procedures Act (1986)]. Testosterone increased mesotocin mRNA expression in both the PVN and BnST, but neither oestradiol, progesterone nor controls had any significant effect. There was no difference among treatments in mesotocin immunohistochemical staining intensity. Mesotocin receptors are primarily located in the lateral septum and we found no significant effect of steroid treatment on mesotocin receptor binding density. For vasotocin, both testosterone and oestradiol increased mRNA expression in the BnST but not the PVN. Together these findings demonstrate that gonadal steroid hormones can upregulate the mesotocin and vasotocin systems in the brain of the domestic hen and the effect of testosterone on mesotocin mRNA expression in the BnST is direct, and not via aromatisation into oestrogen. This hypothesis could be tested by further experiments by blocking aromatase with an aromatase inhibitor.
Research supported by the BBSRC.