Dehydration anorexia is attenuated in oxytocin-deficient mice

Abstract

. Dehydration anorexia is attenuated in oxytocin-deficient mice. Am J Physiol Regul Integr Comp Physiol 288: R1791-R1799, 2005. First published February 17, 2005 doi:10.1152/ajpregu.00860.2004.-Evidence in rats suggests that central oxytocin (OT) signaling pathways contribute to suppression of food intake during dehydration (i.e., dehydration anorexia). The present study examined water deprivation-induced dehydration anorexia in wild-type and OT Ϫ/Ϫ mice. Mice were deprived of food alone (fasted, euhydrated) or were deprived of both food and water (fasted, dehydrated) for 18 h overnight. Fasted wild-type mice consumed significantly less chow during a 60-min refeeding period when dehydrated compared with their intake when euhydrated. Conversely, fasting-induced food intake was slightly but not significantly suppressed by dehydration in OT Ϫ/Ϫ mice, evidence for attenuated dehydration anorexia. In a separate experiment, mice were deprived of water (but not food) overnight for 18 h; then they were anesthetized and perfused with fixative for immunocytochemical analysis of central Fos expression. Fos was elevated similarly in osmo-and volumesensitive regions of the basal forebrain and hypothalamus in wild-type and OT Ϫ/Ϫ mice after water deprivation. OT-positive neurons expressed Fos in dehydrated wild-type mice, and vasopressin-positive neurons were activated to a similar extent in wild-type and OT Ϫ/Ϫ mice. Conversely, significantly fewer neurons within the hindbrain dorsal vagal complex were activated in OT Ϫ/Ϫ mice after water deprivation compared with activation in wild-type mice. These findings support the view that OT-containing projections from the hypothalamus to the hindbrain are necessary for the full expression of compensatory behavioral and physiological responses to dehydration. paraventricular nucleus of the hypothalamus; dorsal vagal complex; water deprivation; vasopressin DEHYDRATION IN RATS INCREASES the expression of mRNAs for c-fos, vasopressin (AVP), and oxytocin (OT) in the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON) (4,5,14,36), and it depletes posterior pituitary stores of AVP and OT (15), while increasing their plasma concentrations (2, 14). Circulating AVP promotes renal retention of water, whereas OT promotes renal excretion of sodium in rats (40). Dehydration also inhibits gastric emptying and food intake (8,30,32,34,42), which together help limit absorption of additional osmoles into the circulation. Finally, dehydration stimulates compensatory drinking of water, when it is available; the subsequent absorption of water into the circulation helps to restore both intracellular and extracellular fluid compartments (31, 34). These adaptive and complementary neuroendocrine, physiological, and behavioral responses to dehydration help to limit its disruptive physiological impact by restoring body fluid homeostasis.In addition to activating magnocellular PVN and SON neurons, osmotic dehydration induced acutely in rats by systemic administration of hypertonic NaCl sol...

Neural network interactions and ingestive behavior control during anorexia

“…These neurons are concentrated within in the dorsal, ventral, and lateral parvicellular parts of the PVH and have extensive projections to the midbrain, hindbrain, and spinal cord. They express a variety of neuropeptides including oxytocin, which has been implicated in some forms of dehydration-anorexia [38].…”

Adenoviral-Mediated Modulation ofSim1Expression in the Paraventricular Nucleus Affects Food Intake

“…The PVN appears to integrate several hypothalamic and extrahypothalamic signals to provide a major hypothalamic output for the regulation of energy intake through its projections to the brainstem (Blevins et al, 2004;Rinaman et al, 2005). Sim1 is also expressed in cells scattered in the anteroventral hypothalamus as well as in the nucleus of the lateral olfactory tract (Balthasar et al, 2005).…”

Enhanced initial and sustained intake of sucrose solution in mice with an oxytocin gene deletion

“…Similarly, dehydration anorexia is markedly attenuated in mice with an OT gene deletion [OT knockout (KO)] (36), and OT KO mice consume more NaCl solution than wild-type (WT) mice after overnight fluid deprivation (2) or after exposure to mild environmental stress (34). However, WT and OT KO mice ingest similar amounts of standard chow under ad libitum baseline conditions, after overnight food deprivation when drinking water is available, and after systemic administration of either cholecystokinin octapeptide or D-fenfluramine (18,36). These findings indicate that neurochemical systems other than OT are sufficient to limit or suppress food intake in mice under such conditions.…”