. 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...

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Transgenic rat models of amyotrophic lateral sclerosis (ALS) have recently been developed. Most assays of ALS-symptoms in these models monitor disease onset accurately, but do not identify individuals that will develop these symptoms before the motor deficits become apparent. Peak bodyweight has recently been shown to indicate affected individuals before motor deficits become apparent. However, it must be determined retrospectively due to weight fluctuation. Here, we report that exploratory activities detected by a photobeam activity system (PAS) and wire mesh ascending test can be used to detect slight motor deficits in the early phase of ALS. Thus, these tests may be used in addition to peak bodyweight to monitor early disease progression and to assay efficacy of new therapeutic interventions.

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