Gastric motility in consious rats given oxytocin and an oxytocin antagonist centrally

Flanagan, Loretta M.; Olson, Beatriz R.; Sved, Alan F.; Verbalis, Joseph G.; Stricker, Edward M.

doi:10.1016/0006-8993(92)90255-8

Cited by 80 publications

(70 citation statements)

References 14 publications

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“…The present study confirmed that OT-immunopositive nerve terminals are closely apposed to GLP-1-positive neurons in the DVC and that these neurons are activated by central infusion of an anorexigenic dose of OT. The OT-containing projection from the PVN to the DVC provides a tonic inhibitory influence over vagally mediated gastric motility that is further amplified by anorexigenic treatments (3,4). Thus experimental treatments that activate central OT signaling pathways may inhibit gastric motility and food intake, at least in part, due to OTmediated recruitment/activation of hindbrain GLP-1 neurons.…”

Section: Discussionmentioning

confidence: 99%

GLP-1 receptor signaling contributes to anorexigenic effect of centrally administered oxytocin in rats

Rinaman

Rothe

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Rinaman, Linda, and Elizabeth E. Rothe. GLP-1 receptor signaling contributes to anorexigenic effect of centrally administered oxytocin in rats. Am J Physiol Regulatory Integrative Comp Physiol 283: R99-R106, 2002. First published March 29, 2002 10.1152/ajpregu.00008.2002.-The present study examined possible interactions between central glucagon-like peptide-1 (GLP-1) and oxytocin (OT) neural systems by determining whether blockade of GLP-1 receptors attenuates OT-induced anorexia and vice versa. Male rats were acclimated to daily 4-h food access. In the first experiment, rats were infused centrally with GLP-1 receptor antagonist or vehicle, followed by an anorexigenic dose of synthetic OT. Access to food began 20 min later. Cumulative food intake was measured every 30 min for 4 h. In the second experiment, rats were infused with OT receptor blocker or vehicle, followed by synthetic GLP-1 [(7-36) amide]. Subsequent food intake was monitored as before. The anorexigenic effect of OT was eliminated in rats pretreated with the GLP-1 receptor antagonist. Conversely, GLP-1-induced anorexia was not affected by blockade of OT receptors. In a separate immunocytochemical study, OT-positive terminals were found closely apposed to GLP-1-positive perikarya, and central infusion of OT activated c-Fos expression in GLP-1 neurons. These findings implicate endogenous GLP-1 receptor signaling as an important downstream mediator of anorexia in rats after activation of central OT neural pathways. food intake; paraventricular nucleus of the hypothalamus; dorsal vagal complex CENTRAL INFUSION of either synthetic oxytocin (OT) or glucagon-like peptide-1 (GLP-1) inhibits deprivationinduced food intake in rats (1,2,13,28,30,31). Hypothalamic OT-and hindbrain GLP-1-containing neurons are activated in rats after various treatments that promote anorexia; such treatments include systemic administration of lithium chloride, lipopolysaccharide, or cholecystokinin octapeptide (16,17,19,32). Furthermore, pharmacological studies provided evidence that central OT and GLP-1 receptor signaling pathways contribute to the anorexigenic effects of several such treatments (5,14,15,25).OT neurons that project to sites within the brain are located in parvocellular subnuclei of the paraventricular nucleus of the hypothalamus (PVN) (27). GLP-1 neurons are located in the hindbrain, within and near caudal levels of the dorsal vagal complex (DVC) (8, 9, 11). Direct, reciprocal neural connections exist between the hypothalamic and hindbrain regions where OT and GLP-1 neurons are located (19,20,24,26). Hypothalamic OT neurons express GLP-1 receptors (12, 33), and central administration of GLP-1 activates c-Fos expression in OT neurons (10). These findings suggest that the anorexigenic effect of centrally administered GLP-1 might result from activation of OT neurons and signaling pathways originating in the PVN. The present study was initiated to test this hypothesis. However, we also considered the possibility that the anorexigenic effect of centrally administer...

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Section: Discussionmentioning

confidence: 99%

GLP-1 receptor signaling contributes to anorexigenic effect of centrally administered oxytocin in rats

Rinaman

Rothe

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The motility in the stomach, ileum and caecum was inhibited, while the motility in colon was stimulated, in several animal species [6][7][8][9][10][11]. When performing this study, we…”

Section: Discussionmentioning

confidence: 99%

“…Intravenous infusion of oxytocin leads to increased colonic peristalsis, and to accelerated gastric emptying of a meal in healthy subjects [3,4], whereas an oxytocin receptor antagonist delays the gastric emptying [5]. In contrast, gastric motility is inhibited in dogs and rats [6,7,8]. Oxytocin relaxes the ileum and caecum, while it has a contracting effect on colon, both in vitro [9,10] and in vivo [ 6,7,11].…”

Section: Introductionmentioning

confidence: 99%

Oxytocin is expressed throughout the human gastrointestinal tract

Ohlsson

Truedsson

Djerf

et al. 2006

Regulatory Peptides

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“…These OT-receptor antagonists have been documented to block a variety of central actions of OT (3,4,(11)(12)(13)(14). Thirty minutes after these treatments, the rats were given i.p.…”

Section: Materuils and Methodsmentioning

confidence: 99%

Central oxytocin inhibition of salt appetite in rats: evidence for differential sensing of plasma sodium and osmolality.

Blackburn

Samson

Fulton

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Sodium chloride ingestion is stimulated during conditions of sodium deficiency to maintain body fluid and electrolyte balance. Recent studies have indicated that salt appetite in rats is often inversely related to peripheral and central secretion of the hormone oxytocin (OT). We studied the potential role of central OT on salt and water ingestion by treating rats intracerebroventricularly with OT conjugated to the A chain of the plant cytotoxin ricn (rAOT) to produce a chronic selective inactivation of brain ceils containing OTreceptive elements. The rats treated with rAOT and control rats treated with the ricin A chain alone were given 5-hr two-bottie (water and 0.5 M NaCI) drinking tests 30 min after they were made hyperosmolar by injections of hypertonic (2 M) mannitol solution, which elevated plasma osmolality but reduced plasma Na+ concentration. In the control rats only water intake was stimulated in response to the induced hyperosmolality, but in the rAOT-treated rats hypertonic mannitol caused a robnst salt appetite as weil as thirst. Analogous results were obtained in rats treated with two different OT-receptor antagonists prior to induction of hyperosmolality with mannitol. In contrast to these results, when hyperosmolalibty was induced by inistration of equivalently hypertonic (1 M) NaCI, which elevated both plasma osmolality and plasma Na4 concentration, only water intake but not salt intake was stimulated in both control and OT-receptor antagonist-treated rats. When salt appetite was stimulated by the physiological stimulns of polyethylene glycol-induced hypovolemia, hypertonic mannitol simiary inhibited salt ingestion in control animals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited subsequent salt ingestion in both groups. These results suggest that salt appetite is regulated by both Na+-and osmolality-sensing mechanisms in rats. In addition, they indicate that central OT likely mediates a significant component of osmolality-related inhibition ofsalt appetite but does not appear to be essential for Na+-related inhibition of this important homeostatic behavior.Salt appetite is a vital homeostatic behavior in many species. The ingestion of salt in response to a perceived body deficit of Na+ is analogous to the ingestion of water by dehydrated animals. Together these two behaviors promote maintenance of body fluid and electrolyte balance within very narrow limits. In rats, ingestion of concentrated NaCl solutions can be induced by diverse experimental manipulations. However, regardless of the paradigm employed, NaCl ingestion is generally most prominent when pituitary oxytocin (OT) release is either low or at basal levels and is almost always inhibited when OT release is stimulated (1). Since central, but not peripheral, administration of OT can inhibit salt appetite in rats, it has been proposed that OT pathways projectingThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accorda...

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Gastric motility in consious rats given oxytocin and an oxytocin antagonist centrally

Cited by 80 publications

References 14 publications

GLP-1 receptor signaling contributes to anorexigenic effect of centrally administered oxytocin in rats

GLP-1 receptor signaling contributes to anorexigenic effect of centrally administered oxytocin in rats

Oxytocin is expressed throughout the human gastrointestinal tract

Central oxytocin inhibition of salt appetite in rats: evidence for differential sensing of plasma sodium and osmolality.

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