Clozapine's functional mesolimbic selectivity is not duplicated by the addition of anticholinergic action to haloperidol: a brain stimulation study in the rat
dc.contributor.author | Walker, Leslie Stern | en_US |
dc.contributor.author | Gardner, Eliot L. | en_US |
dc.contributor.author | Paredes, William | en_US |
dc.date.accessioned | 2006-09-11T17:39:45Z | |
dc.date.available | 2006-09-11T17:39:45Z | |
dc.date.issued | 1993-01 | en_US |
dc.identifier.citation | Gardner, Eliot L.; Walker, Leslie Stern; Paredes, William; (1993). "Clozapine's functional mesolimbic selectivity is not duplicated by the addition of anticholinergic action to haloperidol: a brain stimulation study in the rat." Psychopharmacology 110 (1-2): 119-124. <http://hdl.handle.net/2027.42/46341> | en_US |
dc.identifier.issn | 0033-3158 | en_US |
dc.identifier.issn | 1432-2072 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/46341 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7870870&dopt=citation | en_US |
dc.description.abstract | This study examined whether the anticholinergic potency of the clinically superior antipsychotic drug clozapine contributes to clozapine's anatomically-selective functional inhibition of the mesolimbic dopamine (DA) system, using an electrical brain-stimulation reward (BSR) paradigm in rats that has been previously shown to be highly sensitive to clozapine's mesolimbic functional selectivity. Rats were chronically administered saline, clozapine, haloperidol, or haloperidol plus the anticholinergic compound trihexyphenidyl, and threshold sensitivity of the mesolimbic and nigrostriatal DA systems was assessed using the BSR paradigm, to infer degree of functional DA blockade produced by the chronic drug regimens. Chronic saline produced no change in either DA system. Congruent with previous findings, chronic clozapine powerfully inhibited the mesolimbic DA system but spared the nigrostriatal DA system. Also congruent with previous findings, chronic haloperidol powerfully inhibited both DA systems. Compared to chronic haloperidol alone, chronic haloperidol plus chronic trihexyphenidyl exerted diminished anti-DA action in both the mesolimbic and nigrostriatal DA systems. These results suggest that clozapine's anticholinergic potency is not an adequate explanation for its functional mesolimbic selectivity. | en_US |
dc.format.extent | 814131 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 | Substantia Nigra | en_US |
dc.subject.other | Pharmacology/Toxicology | en_US |
dc.subject.other | Neuroleptic | en_US |
dc.subject.other | ICSS | en_US |
dc.subject.other | Brain Stimulation Reward | en_US |
dc.subject.other | Nigrostriatal | en_US |
dc.subject.other | Trihexyphenidyl | en_US |
dc.subject.other | Schizophrenia | en_US |
dc.subject.other | Acetylcholine | en_US |
dc.subject.other | Atypical | en_US |
dc.subject.other | Mesolimbic | en_US |
dc.subject.other | Antipsychotic | en_US |
dc.subject.other | Psychosis | en_US |
dc.subject.other | Ventral Tegmental Area | en_US |
dc.subject.other | Self-stimulation | en_US |
dc.subject.other | Biomedicine | en_US |
dc.subject.other | Psychiatry | en_US |
dc.subject.other | Haloperidol | en_US |
dc.subject.other | Dopamine | en_US |
dc.subject.other | Clozapine | en_US |
dc.title | Clozapine's functional mesolimbic selectivity is not duplicated by the addition of anticholinergic action to haloperidol: a brain stimulation study in the rat | 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 | Program in Brain and Behavior, Department of Psychiatry, Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461, Bronx, NY, USA; Medical Scientist Training Program and Department of Neuroscience, University of Michigan, 48104, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationother | Program in Brain and Behavior, Department of Psychiatry, Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461, Bronx, NY, USA | en_US |
dc.contributor.affiliationother | Program in Brain and Behavior, Department of Psychiatry, Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461, Bronx, NY, USA; Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461, Bronx, NY, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 7870870 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/46341/1/213_2005_Article_BF02246960.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF02246960 | en_US |
dc.identifier.source | Psychopharmacology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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