Duodenal loading with glucose induces Fos expression in rat brain: selective blockade by devazepide

Author:

Wang Lixin1,Cardin Sylvain2,Martínez Vicente1,Taché Yvette1,Lloyd K. C. Kent3

Affiliation:

1. Center for Ulcer Research and Education/Digestive Disease Research Center, West Los Angeles Veterans Affairs Medical Center, Department of Medicine and Brain Research Institute, University of California, Los Angeles 90073;

2. Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, Tennessee 37232

3. School of Veterinary Medicine, University of California, Davis, California 95616; and

Abstract

The role of CCK in mediating neuronal activity in the brain in response to dietary carbohydrate was measured by detecting Fos immunoreactivity in response to duodenal glucose load in rats after administration of the CCK-A receptor antagonist devazepide. In adult, male Sprague-Dawley rats, infusion for 30 min of 545 mg (2.18 kcal) dextrose through a duodenal cannula induced Fos expression in the nucleus of the solitary tract (NTS), area postrema (AP), lateral division of the central nucleus of the amygdala (CeAL), and the external subnucleus of the lateral parabrachial nucleus (LPBE). Devazepide treatment (1 mg/kg) attenuated Fos expression in the NTS and AP by 81 and 78%, respectively, but not in the CeAL or LPBE. These results indicate that central neuronal activation is elicited by dietary glucose in the intestinal lumen and that activation of neurons in the NTS and AP is mediated by CCK-A receptors.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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