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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Glucose does not activate nonadrenergic, noncholinergic inhibitory neurons in the rat stomach

Departments of ¹Medicine and ²Pharmacology, Georgetown University Medical Center, Washington, DC

Submitted 8 August 2004 ; accepted in final form 1 November 2004

We reported previously that intravenously administered D-glucose acts in the central nervous system to inhibit gastric motility induced by hypoglycemia in anesthetized rats. The purpose of this study was to determine whether this effect is due to inhibition of dorsal motor nucleus of the vagus (DMV) cholinergic motoneurons, which synapse with postganglionic cholinergic neurons, or to excitation of DMV cholinergic neurons, which synapse with postganglionic nonadrenergic, noncholinergic (NANC) neurons, particularly nitrergic neurons. Three approaches were employed: 1) assessment of the efficacy of D-glucose-induced inhibition of gastric motility in hypoglycemic rats with and without inhibition of nitric oxide synthase [10 mg/kg iv nitro-L-arginine methyl ester (L-NAME)], 2) assessment of the efficacy of intravenous bethanechol (30 µg·kg^–1·min^–1) to stimulate gastric motility in hypoglycemic rats during the time of D-glucose-induced inhibition of gastric motility, and 3) determination of c-Fos expression in DMV neurons after intravenous D-glucose was administered to normoglycemic rats. Results obtained demonstrated that L-NAME treatment had no effect on D-glucose-induced inhibition of gastric motility; there was no reduction in the efficacy of intravenous bethanechol to increase gastric motility, and c-Fos expression was not induced by D-glucose in DMV neurons that project to the stomach. These findings indicate that excitation of DMV cholinergic motoneurons that synapse with postganglionic NANC neurons is not a significant contributing component of D-glucose-induced inhibition of gastric motility.

bethanechol; c-Fos expression; hypoglycemia

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