title: Selective contributions of the medial preoptic nucleus to testosterone-dependant regulation of the paraventricular nucleus of the hypothalamus and the HPA axis.
abstract: Previous data have consistently demonstrated an inhibitory effect of androgens on stress-induced hypothalamic-pituitary-adrenal (HPA) responses. Several brain regions may influence androgen-mediated inhibition of the HPA axis, including the medial preoptic area. To test the role of the medial preoptic nucleus (MPN) specifically, we examined in high- and low-testosterone-replaced gonadectomized rats bearing discrete bilateral lesions of the MPN basal and stress-induced indexes of HPA function, and the relative levels of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) mRNA in the amygdala. High testosterone replacement decreased plasma adrenocorticotropin hormone (ACTH) and paraventricular nucleus (PVN) Fos responses to restraint exposure in sham- but not in MPN-lesioned animals. AVP-, but not CRH-immunoreactivity staining in the external zone of the median eminence was increased by testosterone in sham animals, and MPN lesions blocked this increment in AVP. A similar interaction between MPN lesions and testosterone occurred on AVP mRNA levels in the medial nucleus of the amygdala. These findings support an involvement of MPN projections in mediating the AVP response to testosterone in both the medial parvocellular PVN and medial amygdala. We conclude that the MPN forms part of an integral circuit that mediates the central effects of gonadal status on neuroendocrine and central stress responses.
authors.affiliation: Dept. of Cellular and Physiological Sciences, Life Sciences Centre, The Univ. of British Columbia, 2350 Health Sciences Mall, Vancouver, Canada BC V6T 1Z3.
authors.forename: Martin
authors.initials: M
authors.lastname: Williamson
authors.forename: Victor
authors.initials: V
authors.lastname: Viau
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000679:Amygdala / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D000818:Animals; D001127:Arginine Vasopressin / Q000235:genetics / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D004343:Drug Implants; D015870:Gene Expression / Q000187:drug effects; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology*; D007051:Ibotenic Acid / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D009919:Orchiectomy; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000502:physiology*; D011301:Preoptic Area / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013739:Testosterone / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*
chemical_list: D004343:Drug Implants; D016760:Proto-Oncogene Proteins c-fos; D001127:Arginine Vasopressin; D007051:Ibotenic Acid; D013739:Testosterone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone