title: A progestin antagonist blocks vaginocervical stimulation-induced fos expression in neurones containing progestin receptors in the rostral medial preoptic area.
abstract: Vaginocervical stimulation (VCS) has a variety of effects on the brain, physiology and behaviour. Previous work demonstrated that a progestin antagonist blocked neuronal response to VCS (i.e. Fos expression) in the absence of progesterone in some neurones, and suggested that some of the effects of VCS on the brain are mediated by ligand-independent activation of progestin receptors (PRs). Although it had been reported previously that some of the cells in which VCS induces Fos expression also contain PRs, it had not been determined if a progestin antagonist blocked Fos expression in these particular neurones. The purpose of this experiment was to determine if a progestin antagonist decreases Fos expression specifically in cells that also express PRs in the preoptic area and ventromedial hypothalamus. As has been shown previously, VCS increased Fos-immunoreactive (ir) expression in the particular areas studied. In the rostral medial preoptic area, VCS increased Fos expression in cells that coexpressed PRs, as well as in cells that do not. However, in the caudal medial preoptic area, VCS only increased Fos expression in cells that did not coexpress PRs. Injection of the progestin antagonist, RU 486, decreased Fos expression in the rostral, but not caudal medial preoptic area, and it decreased Fos expression only in cells that coexpressed PR-ir. In contrast to a previous report, in the present study, the progestin antagonist did not inhibit VCS-induced Fos expression in the ventromedial hypothalamic area. The results of this experiment suggest that the progestin antagonist inhibits VCS-induced Fos expression in some neurones by blocking PRs, and they provide further support for the idea that VCS influences neuronal response in some cells by ligand-independent activation of PRs in those cells.
authors.affiliation: Center for Neuroendocrine Studies and Neuroscience and Behavior Program, University of Massachusetts, Amherst, MA 01003, USA. blaustein@cns.umass.edu
authors.forename: J D
authors.initials: JD
authors.lastname: Blaustein
authors.forename: B
authors.initials: B
authors.lastname: Gréco
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D002452:Cell Count; D002584:Cervix Uteri / Q000502:physiology; D003307:Copulation / Q000502:physiology; D005260:Female; D006727:Hormone Antagonists / Q000494:pharmacology*; D015735:Mifepristone / Q000494:pharmacology*; D009474:Neurons / Q000737:chemistry / Q000166:cytology / Q000378:metabolism; D010812:Physical Stimulation; D011301:Preoptic Area / Q000737:chemistry / Q000166:cytology / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000096:biosynthesis* / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011980:Receptors, Progesterone / Q000032:analysis* / Q000276:immunology; D014621:Vagina / Q000502:physiology; D014697:Ventromedial Hypothalamic Nucleus / Q000737:chemistry / Q000166:cytology / Q000502:physiology
chemical_list: D000911:Antibodies, Monoclonal; D006727:Hormone Antagonists; D016760:Proto-Oncogene Proteins c-fos; D011980:Receptors, Progesterone; D015735:Mifepristone