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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00008.2002
Submitted on January 9, 2002
Accepted on March 22, 2002
1 Department of Neuroscience, Univ. of Pittsburgh, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: RINAMAN{at}PITT.EDU.
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 cFos 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.
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