The postnatal emergence of dehydration anorexia in rats is temporally associated with the emergence of dehydration-induced inhibition of gastric emptying

Callahan, John B.; Rinaman, Linda

doi:10.1016/s0031-9384(98)00139-5

Cited by 20 publications

(18 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inhibition of vagally mediated gastric emptying by dehydration is associated with increased Fos immunolabeling within the hindbrain DVC in rats (3,28). However, medial subregions of the NST that are activated to express Fos in adult rats after acute osmotic dehydration are not activated in 2-day-old rats (28), and 2-day-old rats do not display dehydration anorexia (3).…”

Section: Effect Of Water Deprivation To Increase Hindbrain Fos Immunomentioning

confidence: 99%

“…However, medial subregions of the NST that are activated to express Fos in adult rats after acute osmotic dehydration are not activated in 2-day-old rats (28), and 2-day-old rats do not display dehydration anorexia (3). Further, the progressive developmental ingrowth of OTimmunopositive fibers within the rat DVC is temporally correlated with the postnatal emergence of dehydration-induced Fos within the DVC, and both are correlated with the postnatal emergence of dehydration anorexia (3,26,28). Thus the inhibitory effect of osmotic dehydration on food intake emerges gradually during postnatal development in rats and closely coincides with the maturation of OT-containing neural projections from the PVN to the DVC.…”

Section: Effect Of Water Deprivation To Increase Hindbrain Fos Immunomentioning

confidence: 99%

See 1 more Smart Citation

Dehydration anorexia is attenuated in oxytocin-deficient mice

Rinaman¹,

Vollmer²,

Karam³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

View full text Add to dashboard Cite

. 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...

show abstract

Section: Effect Of Water Deprivation To Increase Hindbrain Fos Immunomentioning

confidence: 99%

Section: Effect Of Water Deprivation To Increase Hindbrain Fos Immunomentioning

confidence: 99%

Dehydration anorexia is attenuated in oxytocin-deficient mice

Rinaman¹,

Vollmer²,

Karam³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

View full text Add to dashboard Cite

show abstract

“…Specifically, the lack of DVC Fos expression in neonatal rats after HS treatment suggests that plasma hyperosmolality does not recruit DVC neural circuits in neonates, and raises the question of whether dehydration inhibits gastric emptying in neonatal rats. In fact, HS treatment does not delay gastric emptying in rats tested on postnatal Days 4 or 11, but does inhibit gastric emptying on postnatal Day 19 (Callahan & Rinaman, 1998). Thus, the inhibitory effect of dehydration on gastric emptying emerges sometime between postnatal Days 11 and 19.…”

Section: A Functional Model For the Postnatal Emergence Of Hypothalammentioning

confidence: 91%

“…Centrally mediated responses to plasma hyperosmolality in adult rats include compensatory drinking, neurohypophyseal secretion of OT and vasopressin (Stricker & Verbalis, 1986), inhibition of vagally mediated gastric motility and emptying (Flanagan et al, 1989;Flanagan et al, 1992b), and inhibition of food intake (Flanagan, Dohanics, Verbalis, & Stricker, 1992a). The first two responses also occur in neonatal rats (Almli, 1973;Bruno, 1981;Sinding, Robinson, & Seif, 1980), whereas the latter hypophagic response, termed ''dehydration anorexia,'' does not emerge until after the first 2 weeks of postnatal development (Bruno, 1981;Bruno & Hall, 1982;Callahan & Rinaman, 1998).…”

Section: A Functional Model For the Postnatal Emergence Of Hypothalammentioning

confidence: 99%

Ontogeny of hypothalamic-hindbrain feeding control circuits

Rinaman

2006

Dev. Psychobiol.

Self Cite

View full text Add to dashboard Cite

Ingestive behavior is a complex product of distributed central control systems that respond to a diverse array of internal and external sensory stimuli. Relatively little is known regarding the pathways and mechanisms by which relevant signals are conveyed to the neural circuits that ultimately control ingestive motor output. This report summarizes findings regarding the postnatal development of descending hypothalamic inputs to the hindbrain dorsal vagal complex (DVC). Evidence accumulated primarily in rats indicates that descending neural projections from the hypothalamus to the DVC are both structurally and functionally immature at birth. The progressive postnatal maturation of these projections occurs in parallel with newly emerging physiological and behavioral responsiveness to treatments and stimuli that affect food intake in adults. Thus, the postnatal emergence of new feeding controls may reflect the emerging access of these controls to DVC neural circuits.

show abstract

“…A2 neurons seem to be activated in every experimental situation in which food intake is inhibited, including normal satiety [359][360][361][362][363][364]. A2 neurons are recruited in a graded manner in rats after eating, such that larger meals activate larger numbers of A2 neurons [365].…”

Section: Noradrenergic Neuronsmentioning

confidence: 99%

Neuroendocrine control of satiation

Asarian¹,

Bächler

2014

Hormone Molecular Biology and Clinical Investigation

View full text Add to dashboard Cite

Abstract:Eating is a simple behavior with complex functions. The unconscious neuroendocrine process that stops eating and brings a meal to its end is called satiation. Energy homeostasis is mediated accomplished through the control of meal size via satiation. It involves neural integrations of phasic negative-feedback signals related to ingested food and tonic signals, such as those related to adipose tissue mass. Energy homeostasis is accomplished through adjustments in meal size brought about by changes in these satiation signals. The best understood meal-derived satiation signals arise from gastrointestinal nutrient sensing. Gastrointestinal hormones secreted during the meal, including cholecystokinin, glucagon-like peptide 1, and PYY, mediate most of these. Other physiological signals arise from activation of metabolic-sensing neurons, mainly in the hypothalamus and caudal brainstem. We review both classes of satiation signal and their integration in the brain, including their processing by melanocortin, neuropeptide Y/agouti-related peptide, serotonin, noradrenaline, and oxytocin neurons. Our review is not comprehensive; rather, we discuss only what we consider the best-understood mechanisms of satiation, with a special focus on normally operating physiological mechanisms.

show abstract

The postnatal emergence of dehydration anorexia in rats is temporally associated with the emergence of dehydration-induced inhibition of gastric emptying

Cited by 20 publications

References 21 publications

Dehydration anorexia is attenuated in oxytocin-deficient mice

Dehydration anorexia is attenuated in oxytocin-deficient mice

Ontogeny of hypothalamic-hindbrain feeding control circuits

Neuroendocrine control of satiation

Contact Info

Product

Resources

About