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Titolo:
DOPAMINE D2-LIKE SITES IN SCHIZOPHRENIA, BUT NOT IN ALZHEIMERS, HUNTINGTONS, OR CONTROL BRAINS, FOR [H-3] BENZQUINOLINE
Autore:
SEEMAN P; GUAN HC; NOBREGA J; JIWA D; MARKSTEIN R; BALK JH; PICETTI R; BORRELLI E; VANTOL HHM;
Indirizzi:
UNIV TORONTO,DEPT PHARMACOL,MED SCI BLDG,ROOM 4344 TORONTO ON M5S 1A8CANADA UNIV TORONTO,CLARKE INST PSYCHIAT,DEPT PSYCHIAT TORONTO ON M5T 1R8 CANADA UNIV TORONTO,CLARKE INST PSYCHIAT,MOL NEUROBIOL LAB TORONTO ON M5T 1R8 CANADA SANDOZ PHARMA LTD,PRECLIN RES SECT CH-4002 BASEL SWITZERLAND INST GENET & BIOL MOL & CELLULAIRE F-67404 ILLKIRCH GRAFFENS FRANCE
Titolo Testata:
Synapse
fascicolo: 2, volume: 25, anno: 1997,
pagine: 137 - 146
SICI:
0887-4476(1997)25:2<137:DDSISB>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSITRON EMISSION TOMOGRAPHY; C-11 N-METHYLSPIPERONE; RECEPTORS; BINDING; D-2; D1; CLOZAPINE; AFFINITY;
Keywords:
SCHIZOPHRENIA; DOPAMINE DB-LIKE RECEPTOR; SANDOZ GLC 756 DOPAMINE AGONIST; HUNTINGTONS DISEASE; DOPAMINE D2 KNOCKOUT; D4 DOPAMINE RECEPTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
P. Seeman et al., "DOPAMINE D2-LIKE SITES IN SCHIZOPHRENIA, BUT NOT IN ALZHEIMERS, HUNTINGTONS, OR CONTROL BRAINS, FOR [H-3] BENZQUINOLINE", Synapse, 25(2), 1997, pp. 137-146

Abstract

Although the basis of schizophrenia is not known, evidence indicates a possible overactivity of dopamine pathways. In order to detect any new dopamine receptor-like sites which may be altered in schizophrenia,the present study used a new radioligand, a [H-3]benzo[g]quinoline. The receptors were labelled by this ligand in the presence of other drugs to block the known dopamine D1, D2, D3, or D5 receptors (no D4-selective ligands are available to block D4). Using this method, we found that schizophrenia brain striata had elevated levels of a DB-like sitenot detected in control human postmortem brains or in Alzheimer's, Huntington's, or Parkinson's disease brains. The ligand acted as an agonist at this DB-like site, because binding was abolished by guanine nucleotide. The binding of the ligand to the D4 receptor, however, was not sensitive to guanine nucleotide. The site differed from D2 itself, because S- and R-sulpiride were equally potent at the DB-like site. TheDB-like sites were present in rat and mouse brain but were absent in brain slices from transgenic mice where D2 had been knocked out. The abundance of the receptor was not related to premortem use of antipsychotic drugs. Future research should examine the biochemical differencesbetween the D2 dopamine receptor and these DB-like sites in schizophrenia. (C) 1997 Wiley-Liss, Inc.

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Documento generato il 20/01/20 alle ore 16:10:31