| The Parvocellular Vasotocin System of Japanese Quail: A Developmental and Adult Model for the Study of Influences of Gonadal Hormones on Sexually Differentiated and Behaviorally Relevant Neural Circuits Gian Carlo Panzica,1 Jacques Balthazart,2 Marzia Pessatti,1 and Carla Viglietti-Panzica1 1Department of Anatomy, Pharmacology, and Forensic Medicine, Laboratory of Neuroendocrinology, Rita Levi Montalcini Center for Brain Repair, University of Torino, Tornino, Italy; 2Center for Cellular and Molecular Neurobiology, Research Group in Behavioral Neuroendocrinology, University of Liège, Liège, Belgium Abstract
Vasotocin (VT ; the antidiuretic hormone of birds) is synthesized by diencephalic magnocellular neurons projecting to the neurohypophysis. A sexually dimorphic system of VT-immunoreactive (ir) parvocellular elements has been described within the male medial preoptic nucleus (POM) and the nucleus of the stria terminalis, pars medialis (BSTm) . VT-ir fibers are present in many diencephalic and extradiencephalic locations, and quantitative morphometric analyses demonstrated their sexually dimorphic distribution in regions involved in the control of different aspects of reproduction. Moreover, systemic or intracerebroventricular injections of VT markedly inhibit the expression of some aspects of male sexual behavior. In adult animals, circulating levels of testosterone (T) have a profound influence on the VT immunoreactivity within BSTm, POM, and lateral septum. Castration markedly decreases the immunoreaction, whereas T-replacement therapy restores a situation similar to the intact birds. We observed no changes in gonadectomized females treated with T. These changes parallel similar changes in male copulatory behavior (not present in castrated male quail, fully expressed in castrated, T-treated males) . The restoration by T of the VT immunoreactivity in castrated male quail could be fully mimicked by a treatment with estradiol (E2) , suggesting that the aromatization of T into E2 may play a key limiting role in both the activation of male sexual behavior and the induction of VT synthesis. This dimorphism has an organizational nature: administration of E2 to quail embryos (a treatment that abolishes male sexual behavior) results in a dramatic decrease of the VT immunoreactivity in sexually dimorphic regions. Conversely, the inhibition of E2 synthesis during embryonic life (a treatment that stimulates the expression of male copulatory behavior in treated females exposed in adulthood to T) results in a malelike distribution of VT immunoreactivity. The VT parvocellular system of the Japanese quail can therefore be considered an accurate marker of the sexual differentiation of brain circuits mediating copulatory behavior and could be a very sensitive indicator of the activity of estrogenlike substances on neural circuits. Key words: avian brain, copulatory behavior, development, sexual dimorphism, vasotocin. Environ Health Perspect 110(suppl 3) :423-428 (2002) . http://ehpnet1.niehs.nih.gov/docs/2002/suppl-3/423-428panzica/abstract.html
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