Dehydration-induced drinking decreases Fos expression in hypothalamic paraventricular neurons expressing vasopressin but not corticotropin-releasing hormone

Abstract

Wotus C, Arnhold MM, Engeland WC. Dehydration-induced drinking decreases Fos expression in hypothalamic paraventricular neurons expressing vasopressin but not corticotropin-releasing hormone. Am J Physiol Regul Integr Comp Physiol 292: R1349 -R1358, 2007. First published October 26, 2006; doi:10.1152/ajpregu.00304.2006 rats exhibit a rapid suppression of plasma corticosterone following drinking. The present study monitored Foslike immunoreactivity (Fos) to assess the effect of WR-induced drinking on the activity of vasopressin (VP)-positive magnocellular and parvocellular neurons and corticotropin-releasing hormone (CRH)-positive parvocellular neurons in the paraventricular nucleus of the hypothalamus. Adult male rats received water for 30 min (WR) in the post meridiem (PM) each day for 6 days and were killed without receiving water or at 1 h after receiving water for 15 min. In WR rats, Fos increased in VP magnocellular and parvocellular neurons but not CRH neurons. After drinking, Fos was reduced in VP magnocellular and parvocellular neurons but did not change in CRH neurons. To assess the severity of osmotic stress, rats were sampled throughout the final day of WR. Plasma osmolality, hematocrit and plasma VP were increased throughout the day before PM rehydration, and plasma ACTH and corticosterone were elevated at 1230 and 1430, respectively, showing that WR activates hypothalamic-pituitary-adrenal activity during the early PM before the time of rehydration. To determine the effects of WR-induced drinking on CRH neurons activated by acute stress, WR rats underwent restraint. Restraint increased plasma ACTH and corticosterone and Fos in CRH neurons; although rehydration reduced plasma ACTH and Fos expression in VP neurons, Fos in CRH neurons was not affected. These results suggest that inhibition of VP magnocellular and parvocellular neurons, but not CRH parvocellular neurons, contributes to the suppression of corticosterone after WR-induced drinking.Fos; dehydration; rehydration; magnocellular neurons; parvocellular neurons THE HYPOTHALAMIC-pituitary-adrenal (HPA) response to stress is initiated by the activation of hypophysiotrophic neurons in the paraventricular nucleus (PVN) of the hypothalamus. Release of the peptides corticotropin-releasing hormone (CRH) and vasopressin (VP) from PVN parvocellular neurons in the hypophyseal portal blood stimulates the release of ACTH (46, 55) from the anterior pituitary, which subsequently stimulates the production and release of glucocorticoids from the adrenal cortex. Suppression of this neuroendocrine response has been shown to occur through hormonal negative feedback, in which glucocorticoids act at the brain and pituitary to limit their own production (10, 32). However, studies in rats have shown that the act of drinking after water restriction results in a rapid decrease in plasma corticosterone, the primary glucocorticoid in the rat (21,35,61). These data suggest that signals associated with satiety, or with drive reduction, may have the ability to activate neuro...

Sodium deprivation and salt intake activate separate neuronal subpopulations in the nucleus of the solitary tract and the parabrachial complex

“…After just 1 hour, c‐Fos immunoreactivity disappeared in the majority of these neurons. A similarly rapid decrease in c‐Fos‐immunoreactivity has been observed in a group of dehydration‐activated neurons in the hypothalamus following an analogous sequence of water deprivation and brief access to water (Wotus et al,2007). The inactivation of HSD2 neurons after salt ingestion may be mediated by salt‐activated neurons in the surrounding NTS and AP, either directly or via inhibitory interneurons (see Sequeira et al,2006).…”

Neuroendocrine‐Autonomic Integration in the Paraventricular Nucleus: Novel Roles for Dendritically Released Neuropeptides

“…These two complementary PVN outputs act in concert at the level of the kidneys to properly modulate water and Na + reabsorption/excretion, restoring fluid and electrolyte homeostasis . Moreover, disturbances of fluid homeostasis also result in the activation of CRH neurones with the concomitant engagement of the hypothalamic‐pituitary‐adrenal axis , thus contributing to a multimodal homeostatic response to this type of physiological stressors. Although the general neuroanatomical, neurochemical and physiological features of these neurosecretory and sympathetic responses evoked during an osmotic/fluid challenge are well characterised , knowledge about how the activities of these distinct neuronal populations are coordinated, and whether this coordination results from local integrative processes within the PVN, is largely absent.…”

Chronic dehydration affects hydroelectrolytic equilibrium and adrenal gland morphology in wistar rat: comparison with <i>Gerbillus tarabuli</i>

“…Indeed, it was found (not bublished results) that the plasma level of the primary glucocorticoid (cortisol) in G. tarabuli was comparatively high (292±51 ng/ml), with the same essay method the plasma corticosterone levels in laboratory rat under basal conditions had been estimated to 28.8±7.9ng/ml [23]. In their interesting study Wotus et al, 2007 have shown a positive correlation between plasma levels of corticosterone and the hypothalamic hormone, vasopressin (AVP) in dehydrated rats [24]. This evidence may constitute another argument in favour of a potent steroidogenesis activity; bearing in mind that plasma AVP concentrations were higher in desert rodents than in laboratory rats, as was…”