Document Detail


Effect of CCK pretreatment on the CCK sensitivity of rat polymodal gastric vagal afferent in vitro.
MedLine Citation:
PMID:  10950839     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To prevent the blood-borne interference and reflex actions via neighboring organs and the central nervous system, the study was conducted in an in vitro isolated stomach-gastric vagus nerve preparation obtained from overnight-fasted, urethan-anesthetized rats. Afferent unit action potentials were recorded from the gastric branch of the vagus nerve. The left gastric artery was catheterized for intra-arterial injection. In vitro we found that 1) 55/70 gastric vagal afferents (GVAs) were polymodal, responding to CCK-8 and mechanical stimuli, 13 were mechanoreceptive, and 2 were CCK-responsive; 2) sequential or randomized intra-arterial injections of CCK-8 (0.1-200 pmol) dose-dependently increased firing rate and reached the peak rate at 100 pmol; 3) the action was suppressed by CCK-A (Devazepide) but not by CCK-B (L-365,260) receptor antagonist; 4) neither antagonist blocked the mechanosensitivity of GVA fibers. These results are consistent with corresponding in vivo well-documented findings. Histological data indicate that the layered structure of the stomach wall was preserved in vitro for 6-8 h. Based on these results, it seems reasonable to use the in vitro preparation for conducting a study that is usually difficult to be performed in vivo. For instance, because there was no blood supply in vitro, the composition of the interstitial fluid, i.e., the ambient nerve terminals, can be better controlled and influenced by intra-arterial injection of a defined solution. Here we report that acutely changing the ambient CCK level by a conditioning stimulus (a preceding intra-arterial injection of increasing doses of CCK-8) reduced the CCK sensitivity of GVA terminals to a subsequent test stimulus (a constant dose of CCK-8 intra-arterial injection).
Authors:
J Y Wei; Y H Wang
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  279     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2000 Sep 
Date Detail:
Created Date:  2000-09-19     Completed Date:  2000-09-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  E695-706     Citation Subset:  IM; S    
Affiliation:
Digestive Diseases Division, Department of Medicine, Center for Ulcer Research and Education/Digestive Diseases Research Center and Brain Research Institute, University of California Los Angeles School of Medicine, 90095, USA.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / drug effects
Animals
Cholecystokinin / administration & dosage,  metabolism,  pharmacology*
Electrophysiology
Injections, Intra-Arterial
Male
Mechanoreceptors / physiology
Neurons, Afferent / drug effects*
Physical Stimulation
Rats
Rats, Sprague-Dawley
Receptor, Cholecystokinin A
Receptor, Cholecystokinin B
Receptors, Cholecystokinin / antagonists & inhibitors
Stomach / anatomy & histology,  innervation
Vagus Nerve / cytology,  drug effects*
Grant Support
ID/Acronym/Agency:
DK-48476/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Receptor, Cholecystokinin A; 0/Receptor, Cholecystokinin B; 0/Receptors, Cholecystokinin; 9011-97-6/Cholecystokinin

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


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