Effects of clonidine and some α-adrenergic antagonists alone and in combination on schedule-controlled behavior in pigeons and mice
dc.contributor.author | Katz, Jonathan L. | en_US |
dc.date.accessioned | 2006-09-11T17:46:27Z | |
dc.date.available | 2006-09-11T17:46:27Z | |
dc.date.issued | 1984-04 | en_US |
dc.identifier.citation | Katz, Jonathan L.; (1984). "Effects of clonidine and some α-adrenergic antagonists alone and in combination on schedule-controlled behavior in pigeons and mice." Psychopharmacology 83(1): 38-43. <http://hdl.handle.net/2027.42/46431> | en_US |
dc.identifier.issn | 0033-3158 | en_US |
dc.identifier.issn | 1432-2072 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/46431 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=6146155&dopt=citation | en_US |
dc.description.abstract | Schedule-controlled responding was maintained under multiple fixed-interval, fixed-ratio schedules in pigeons and single fixed-ratio schedules in mice. In pigeons, clonidine, an α 2 -receptor agonist, produced dose-related decreases in responding under both fixed-interval and fixedratio schedules; fixed-interval responding was decreased at a lower dose than fixed-ratio responding. Low to intermediate doses of yohimbine, an α 2 -receptor antagonist, increased responding under the fixed-interval schedule without appreciably affecting responding under the fixed-ratio schedule; higher doses decreased responding under both schedules. In mice, both clonidine and yohimbine produced dose-related decreases in responding under fixed-ratio schedules. Decreases in response rates produced by clonidine were antagonized by low to intermediate doses of yohimbine. Decreases in response rates under fixed-ratio schedules produced by yohimbine were antagonized only slightly, if at all, by clonidine. Under the fixed-interval schedule, clonidine potentiated the response-rate increasing effects of intermediate doses of yohimbine and slightly antagonized the rate-decreasing effects. Although some effects of clonidine were antagonized by yohimbine, at no dose combination did performances completely resemble control performances. Prazosin, an α 1 -receptor antagonist, was ineffective both when administered alone and as an antagonist of the effects of clonidine. The behavioral effects of clonidine appeared to be mediated by α 2 rather than α 1 receptors. Additionally, yohimbine appears to have significant behavioral effects other than α 2 -antagonist actions. | en_US |
dc.format.extent | 759199 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Springer-Verlag | en_US |
dc.subject.other | α-Adrenergic Agents | en_US |
dc.subject.other | Prazosin | en_US |
dc.subject.other | Yohimbine | en_US |
dc.subject.other | Psychiatry | en_US |
dc.subject.other | Biomedicine | en_US |
dc.subject.other | Pharmacology/Toxicology | en_US |
dc.subject.other | Clonidine | en_US |
dc.subject.other | Schedule-controlled Behavior | en_US |
dc.subject.other | Pigeons | en_US |
dc.subject.other | Mice | en_US |
dc.title | Effects of clonidine and some α-adrenergic antagonists alone and in combination on schedule-controlled behavior in pigeons and mice | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Psychiatry | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Chemistry | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Harvard Medical School and University of Michigan Medical School, Cambridge, USA; NIDA Addiction Research Center, P.O. Box 5180, 21224, Baltimore, MD, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 6146155 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/46431/1/213_2004_Article_BF00427419.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF00427419 | en_US |
dc.identifier.source | Psychopharmacology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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