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dc.contributor.advisorPorreca, Franken_US
dc.contributor.authorJiang, Qi, 1957-
dc.creatorJiang, Qi, 1957-en_US
dc.date.accessioned2013-05-16T09:42:15Z
dc.date.available2013-05-16T09:42:15Z
dc.date.issued1989en_US
dc.identifier.urihttp://hdl.handle.net/10150/291819
dc.description.abstractThe 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.
dc.language.isoen_USen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © 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.en_US
dc.subjectClonidine.en_US
dc.subjectGastrointestinal system -- Motility.en_US
dc.subjectNeurotransmitters.en_US
dc.subjectMice -- Physiology.en_US
dc.titleSite of clonidine action to inhibit gut propulsion in mice: Demonstration of a central componenten_US
dc.typetexten_US
dc.typeThesis-Reproduction (electronic)en_US
dc.identifier.oclc22439561en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelmastersen_US
dc.identifier.proquest1336694en_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplinePharmacologyen_US
thesis.degree.nameM.S.en_US
dc.identifier.bibrecord.b17428543en_US
refterms.dateFOA2018-06-18T09:58:42Z
html.description.abstractThe 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.


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