Reduction of Food Intake and Morphine Analgesia by Central GlybenclamidePharmacology Biochemistry and Behavior (1993)
Previous research has indicated the presence of a reciprocal relationship between food intake and opioid-mediated analgesia. We believe the cellular candidate most likely acting as a common mediator of both ingestive and nociceptive behaviors is the ATP-sensitive K+ channel (K+ATP). This ion channel appears to be opened by mu and delta1 opioid receptor agonists in the service of analgesia, and closed as cellular ATP availability rises. To further examine the role of the K+ATP in the relationship between feeding and opioid function, we administered 80 nmol of glybenclamide (a K+ATP antagonist) to male SD rats via the lateral ventricle. Chow consumption in the treated animals was significantly reduced over the following 48 h (F = 2.62, p < 0.013), with the peak effect (78% of control) occurring at 6 h. In the tail-flick test, 4 mg/kg morphine sulfate provided analgesia of 42.38 ± 8.4% and 18.89 ± 7.67% in vehicle and treated animals, respectively (p < 0.05, n = 8/group, one-tailed t-test). These results support the hypothesis that food intake and analgesia are reciprocally modulated through activity at the K+ATP.
- food intake,
- morphine analgesia,
- central glybenclamide
Publication DateSeptember, 1993
Citation InformationDavid S. Roane and Nancy Boyd. "Reduction of Food Intake and Morphine Analgesia by Central Glybenclamide" Pharmacology Biochemistry and Behavior Vol. 46 Iss. 1 (1993) p. 205 - 207 ISSN: 1873-5177
Available at: http://works.bepress.com/david-s-roane/23/