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    Site of clonidine action to inhibit gut propulsion in mice: Demonstration of a central component

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    Author
    Jiang, Qi, 1957-
    Issue Date
    1989
    Keywords
    Clonidine.
    Gastrointestinal system -- Motility.
    Neurotransmitters.
    Mice -- Physiology.
    Advisor
    Porreca, Frank
    
    Metadata
    Show full item record
    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    The role of supraspinal, spinal and peripheral alpha-2 adrenoceptors in the regulation of gastrointestinal motility in mice was investigated using anatomically site specific administration of clonidine and adrenoceptor antagonists. Clonidine produced a dose-dependent inhibition of gastrointestinal transit when given by the i.c.v., i.th., or s.c. routes, and was most potent when given i.c.v. Yohimbine, an alpha-2 adrenoceptor antagonist, but not the alpha-1 antagonist prazosin, antagonized the antitransit effects of clonidine. Yohimbine was most potent in antagonizing i.c.v. clonidine; increased doses of the i.c.v. antagonist were required when the agonist was given s.c. After transection of the spinal cord, i.th. clonidine failed to produce an antitransit effect. Additionally, the i.c.v. potency of clonidine decreased approximately 7-fold in spinally-transected mice. The data suggest that the antitransit effects of clonidine occur through actions at alpha-2 adrenoceptors located at both supraspinal and peripheral sites.
    Type
    text
    Thesis-Reproduction (electronic)
    Degree Name
    M.S.
    Degree Level
    masters
    Degree Program
    Graduate College
    Pharmacology
    Degree Grantor
    University of Arizona
    Collections
    Master's Theses

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