Intraventricular 2-deoxy-D-glucose induces Fos expression by hypothalamic vasopressin, but not oxytocin neurons

The glucostatic theory supports the role of central and peripheral substrat e "sensors" in monitoring cellular glucose metabolism. Induction of hyperph agia and hyperglycemia by intracerebroventricular (i.c.v.) delivery of drug s inhibiting glucose uptake or oxidation suggests that glucose "sensors" ar e accessible from the cerebroventricular system. Although glucopenia elevat es neurohypophyseal vasopressin (VP) and oxytocin (OXY) secretion and induc es c-fos expression by hypothalamic paraventricular (PVN) and supraoptic (S ON) neurons, the origin of glucoprivic regulatory signals impinging upon th ese cell populations is unclear. The following study evaluated immunolabeli ng of hypothalamic VP and OXY neurons for the nuclear transcription factor, Fos, following systemic vs. i.c.v. delivery of the glucose antimetabolite, 5-deoxy-D-glucose (2DG), Intraperitoneal drug treatment resulted in Fos ex pression by a high proportion of AVP- and OXY-ir neurons in the PVN and SON , whereas i.c.v. antimetabolite administration resulted in immunostaining o f a smaller proportion of AVP neurons and a lack of colabeling of OXY neuro ns in both sites. These results suggest that decreased glucose metabolism w ithin the periventricular CNS is a stimulus for central mechanisms that act ivate the Fos stimulus-transcription cascade in a discrete subpopulation of VP neurons in the PVN and SON. Alternatively, the absence of demonstrable Fos expression by OXY neurons in the same structures suggests that the func tional status of these cells is regulated by glucoprivic stimuli of periphe ral and/or nonperiventricular central origin. (C) 2000 Elsevier Science Inc .