Document Detail


Activation of submucosal but not myenteric plexus of the gastrointestinal tract accompanies reduction of food intake by camostat.
MedLine Citation:
PMID:  18620003     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It has been shown in the rat that endogenous cholecystokinin (CCK), released in response to the non-nutrient trypsin inhibitor camostat, reduces food intake at meals and increases Fos-like immunoreactivity (Fos-LI; a marker for neuronal activation) in the dorsal vagal complex (DVC) of the hindbrain but not the myenteric plexus of the duodenum and jejunum. Experiment 1: We examined Fos-LI in the myenteric and the submucosal plexuses of the gut in response to orogastric gavage of camostat in rats. As we reported previously, camostat failed to increase Fos-LI in the myenteric plexus. We show here that camostat increased Fos-LI in the submucosal plexus of the duodenum and jejunum. Camostat also increased Fos-LI in the DVC. Experiment 2: Pretreatment with devazepide, a specific CCK(1) receptor antagonist abolished camostat-induced Fos-LI in the submucosal plexus and the DVC. Experiment 3: Bilateral subdiaphragmatic vagotomy reduced camostat-induced Fos-LI in the submucosal plexus approximately 40% and abolished it in the DVC. Conclusions: Activation of the submucosal plexus by cholecystokinin at the CCK(1) receptor accompanies stimulation of the dorsal vagal complex of the hindbrain and inhibition of food intake. Unlike the submucosal plexus, activation of the myenteric plexus is not necessary for cholecystokinin's influence on the dorsal vagal complex and food intake. The lack of activation in the myenteric plexus after camostat stimulation, in contrast to nutrient releasers of CCK such as oleate, suggests that intestinal stimulants can either release different amounts of CCK or cause release of CCK from I cells with different molecular forms of CCK. This would suggest that CCK-8 is released by camostat and is not able to travel to the myenteric plexus while a more stable form of CCK such as CCK-58 can travel to this site that is further away from the I cell.
Authors:
Shannon J Raboin; Joseph R Reeve; Marvis S Cooper; Gary M Green; Ayman I Sayegh
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2008-06-23
Journal Detail:
Title:  Regulatory peptides     Volume:  150     ISSN:  0167-0115     ISO Abbreviation:  Regul. Pept.     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-09-15     Completed Date:  2008-11-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8100479     Medline TA:  Regul Pept     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  73-80     Citation Subset:  IM    
Affiliation:
Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, Alabama, United States.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cholecystokinin / pharmacology
Devazepide / pharmacology
Eating / drug effects*
Gabexate / analogs & derivatives*,  pharmacology
Gastrointestinal Tract / drug effects*,  metabolism
Hormone Antagonists / pharmacology
Models, Biological
Myenteric Plexus / metabolism*
Proto-Oncogene Proteins c-fos / metabolism
Rats
Rats, Sprague-Dawley
Receptors, Cholecystokinin / physiology
Solitary Nucleus / drug effects
Submucous Plexus / drug effects*,  metabolism
Vagus Nerve / drug effects
Grant Support
ID/Acronym/Agency:
DK-41301/DK/NIDDK NIH HHS; P20MD000195-05/MD/NCMHD NIH HHS; R01-DK33850/DK/NIDDK NIH HHS; S06/GM08091-31/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Hormone Antagonists; 0/Proto-Oncogene Proteins c-fos; 0/Receptors, Cholecystokinin; 103420-77-5/Devazepide; 39492-01-8/Gabexate; 59721-28-7/FOY 305; 9011-97-6/Cholecystokinin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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