Site of clonidine action to inhibit gut propulsion in mice: Demonstration of a central component
dc.contributor.advisor | Porreca, Frank | en_US |
dc.contributor.author | Jiang, Qi, 1957- | |
dc.creator | Jiang, Qi, 1957- | en_US |
dc.date.accessioned | 2013-05-16T09:42:15Z | |
dc.date.available | 2013-05-16T09:42:15Z | |
dc.date.issued | 1989 | en_US |
dc.identifier.uri | http://hdl.handle.net/10150/291819 | |
dc.description.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. | |
dc.language.iso | en_US | en_US |
dc.publisher | The University of Arizona. | en_US |
dc.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. | en_US |
dc.subject | Clonidine. | en_US |
dc.subject | Gastrointestinal system -- Motility. | en_US |
dc.subject | Neurotransmitters. | en_US |
dc.subject | Mice -- Physiology. | en_US |
dc.title | Site of clonidine action to inhibit gut propulsion in mice: Demonstration of a central component | en_US |
dc.type | text | en_US |
dc.type | Thesis-Reproduction (electronic) | en_US |
dc.identifier.oclc | 22439561 | en_US |
thesis.degree.grantor | University of Arizona | en_US |
thesis.degree.level | masters | en_US |
dc.identifier.proquest | 1336694 | en_US |
thesis.degree.discipline | Graduate College | en_US |
thesis.degree.discipline | Pharmacology | en_US |
thesis.degree.name | M.S. | en_US |
dc.identifier.bibrecord | .b17428543 | en_US |
refterms.dateFOA | 2018-06-18T09:58:42Z | |
html.description.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. |