Pathways of Fos expression in locus ceruleus, dorsal vagal complex, and PVN in response to intestinal lipid
H. Monnikes, G. Lauer, C. Bauer, J. Tebbe, T. T. Zittel and R. Arnold Department of Internal Medicine, Philipps-University of Marburg, Germany. Exogenous cholecystokinin (CCK) injected peripherally mimics effects of lipid entering the intestine on food intake and gastric motility via vagal afferents...
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Published in | American journal of physiology. Regulatory, integrative and comparative physiology Vol. 273; no. 6; pp. 2059 - R2071 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.12.1997
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Subjects | |
Online Access | Get full text |
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Summary: | H. Monnikes, G. Lauer, C. Bauer, J. Tebbe, T. T. Zittel and R. Arnold
Department of Internal Medicine, Philipps-University of Marburg, Germany.
Exogenous cholecystokinin (CCK) injected peripherally mimics effects of
lipid entering the intestine on food intake and gastric motility via vagal
afferents and induces c-fos expression in the locus ceruleus complex (LCC),
nucleus of the solitary tract (NTS), area postrema (AP), and
paraventricular nucleus (PVN). However, the role of peripheral endogenous
CCK in induction of c-fos expression in the brain at ingestion of nutrients
is controversial. In awake rats, intraduodenal lipid infusion markedly
increased Fos protein-like immunoreactivity (FLI) in these brain nuclei.
Perivagal capsaicin pretreatment reduced the increase of FLI in the LCC,
NTS, and PVN by 66-86% and in the AP by 46%. The CCK-A receptor antagonist
MK-329 (0.1 mg/kg i.p.) diminished the FLI increase in LC, NTS, AP, and PVN
by 39-100%; the CCK-B receptor antagonist L-365,260 reduced the increased
FLI in the AP by 54%. After capsaicin pretreatment, both CCK antagonists
had additional inhibitory effects only on FLI in the AP. These findings
suggest that entry of lipid into the intestine activates c-fos in the LCC,
NTS, and PVN predominantly via CCK-A receptors on vagal afferents and in
the AP via vagal and nonvagal pathways, as well as CCK-B and CCK-A
receptors. |
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Bibliography: | S20 1997072547 |
ISSN: | 0002-9513 0363-6119 2163-5773 1522-1490 |
DOI: | 10.1152/ajpregu.1997.273.6.r2059 |