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1 Department of Medicine, Georgetown University Medical Center, Washington, DC, USA
2 Department of Pharmacology, Georgetown University Medical Center, Washington, DC, USA
* To whom correspondence should be addressed. E-mail: verbalis{at}georgetown.edu.
We reported previously that i.v. administered D-glucose acts in the CNS 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 motor neurons that synapse with postganglionic cholinergic neurons, or to excitation of DMV cholinergic neurons that synapse with postganglionic (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 (L-NAME, 10 mg/kg, i.v.); (2) assessment of the efficacy of i.v. bethanechol (30 µg/kg/min) to stimulate gastric motility in hypoglycemic rats during the time of D-glucose-induced inhibition of gastric motility; and (3) determination of cFos expression in DMV neurons after i.v. 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 i.v. bethanechol to increase gastric motility; and cFos expression was not induced by D-glucose in DMV neurons that project to the stomach. These findings indicate that excitation of DMV cholinergic motor neurons that synapse with postganglionic NANC neurons is not a significant contributing component of D-glucose-induced inhibition of gastric motility.
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