Chronic haloperidol treatment increased calcium-dependent phosphorylation in rat striatum
dc.contributor.author | Lao, Yuen-Sum | en_US |
dc.contributor.author | Gnegy, Margaret E. | en_US |
dc.date.accessioned | 2006-04-07T17:55:22Z | |
dc.date.available | 2006-04-07T17:55:22Z | |
dc.date.issued | 1982-01-04 | en_US |
dc.identifier.citation | Lao, Yuen-Sum, Gnegy, Margaret E. (1982/01/04)."Chronic haloperidol treatment increased calcium-dependent phosphorylation in rat striatum." Life Sciences 30(1): 21-28. <http://hdl.handle.net/2027.42/24079> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6T99-475WMFR-246/2/613276ff913476559f2aa8a588b98ea7 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/24079 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=6275231&dopt=citation | en_US |
dc.description.abstract | In previous studies, we observed that when rats were chronically treated with haloperidol, there was a significant increase of calmodulin activity in their striatal membranes. Calmodulin is knwon to modulate calcium-dependent protein phosphorylation in neural membranes. In the present study, we found that the total 32P-incorporation in the striatal proteins from chronic haloperidol-treated rats was significantly increased in comparison to saline-treated rats. A majority of the phosphorylation was attributed to the calcium-mediated activity, since it could be blocked by a calcium chelating agent (EGTA). By using EGTA to inhibit phosphorylation, the results indicated that the haloperidol-treated rats had approximately 3.5-fold greater Ca++-dependent protein kinase activity than the saline-treated rats. Exogenous calcium alone was insufficient to stimulate phosphorylation in the haloperidol-treated rats to the same magnitude as in the saline-treated rats. Calmodulin may be required. 32P-incorporation of two striatal proteins at molecular weight 40 and 52 kilodaltons were markedly stimulated by calcium. Cyclic AMP-mediated phosphorylation seemed to take only a small part in the alteration of total phosphorylation. Therefore, the increase of calmodulin activity and calcium-dependent phosphorylation appears to play a major role in the drug-induced dopamine receptor supersensitivity in rat striatum. | en_US |
dc.format.extent | 446590 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Chronic haloperidol treatment increased calcium-dependent phosphorylation in rat striatum | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Natural Resources and Environment | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Ecology and Evolutionary Biology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Pharmacology, Creighton University Medical School, Omaha, NE 68178, USA; University of Michigan Medical School, Ann Arbor, MI 48109, USA | en_US |
dc.contributor.affiliationum | Department of Pharmacology, Creighton University Medical School, Omaha, NE 68178, USA; University of Michigan Medical School, Ann Arbor, MI 48109, USA | en_US |
dc.identifier.pmid | 6275231 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/24079/1/0000332.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0024-3205(82)90631-2 | en_US |
dc.identifier.source | Life Sciences | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.