title: Oxytocin and vasopressin neurones in principal and accessory hypothalamic magnocellular structures express Fos-immunoreactivity in response to acute glucose deprivation.
abstract: Neurohypophyseal secretion of oxytocin and vasopressin is elevated in response to decreased systemic glucose availability. In these studies, dual-label immunocytochemistry was used to identify hypothalamic neuropeptidergic magnocellular neurones that are transcriptionally activated in response to glucose substrate imbalance. Two h after i.p. injection of the glucose antimetabolite, 2-deoxy-D-glucose (2DG), or the vehicle, saline, groups of adult male rats were anaesthetized by i.p. injection with sodium pentobarbital and killed by transcardial perfusion. Sections (25 microm) through anterior and tuberal levels of the hypothalamus were processed for nuclear Fos- and cytoplasmic neuropeptide immunoreactivity (-ir). A high proportion of oxytocin-ir neurones in the supraoptic, paraventricular, and adjunct structures, including the anterior commissural, periventricular magnocellular, posterior perifornical, recurrent supraoptic, medial forebrain, and circular nuclei, were colabelled for nuclear Fos-ir following administration of 2DG. Large numbers of vasopressin neurones in the supraoptic, circular, posterior perifornical, and medial forebrain nuclei, and posterior magnocellular division and posterior subnucleus of the paraventricular nucleus were also immunostained for Fos in rats injected with the antimetabolite. These results show that decreased glucose metabolism is a stimulus for activation of the Fos stimulus-transcription cascade within oxytocin-and vasopressin-immunopositive neurones in several hypothalamic loci, findings that reflect activation of the Fos-stimulus transcription cascade within large proportions of these cell populations during this metabolic challenge. These data suggest that both peripheral hormonal and central modulatory functions of these neuropeptidergic neurones may be influenced by cellular glucose availability.
authors.affiliation: Division of Basic Pharmaceutical Sciences, College of Pharmacy, University of Louisiana at Monroe, Monroe, LA 71209-0470, USA.
authors.forename: K P
authors.initials: KP
authors.lastname: Briski
authors.forename: J A
authors.initials: JA
authors.lastname: Brandt
mesh_terms: D000818:Animals; D002467:Cell Nucleus / Q000737:chemistry; D003593:Cytoplasm / Q000737:chemistry; D003847:Deoxyglucose / Q000494:pharmacology; D005947:Glucose / Q000037:antagonists & inhibitors* / Q000378:metabolism; D007031:Hypothalamus / Q000166:cytology*; D007150:Immunohistochemistry; D008297:Male; D009474:Neurons / Q000737:chemistry* / Q000187:drug effects / Q000502:physiology; D010121:Oxytocin / Q000032:analysis* / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014667:Vasopressins / Q000032:analysis* / Q000378:metabolism
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D014667:Vasopressins; D010121:Oxytocin; D003847:Deoxyglucose; D005947:Glucose