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The effect of haloperidol feeding on dopamine receptor number in ten mouse strains
Author(s) -
Belmaker Robert H.,
Bannet Jacob,
BrecherFride Ester,
Yanai Joseph,
Ebstein Richard P.
Publication year - 1981
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1111/j.1399-0004.1981.tb00725.x
Subject(s) - tardive dyskinesia , haloperidol , dopamine receptor , receptor , endocrinology , medicine , dyskinesia , pharmacogenetics , dopamine , pharmacology , biology , genotype , genetics , schizophrenia (object oriented programming) , gene , psychiatry , disease , parkinson's disease
Mean DA receptor number in rats rises markedly after chronic haloperidol treatment, and this rise is accompanied by a significantly increased variance. The rise in DA receptor number has been proposed as a molecular model of human tardive dyskinesia. Since human tardive dyskinesia may involve pharmacogenetic susceptibility, ten inbred mouse strains were treated for 3 weeks with haloperidol and caudate DA receptor number was determined 4 days after cessation of feeding. Some strains showed much larger rises in DA receptor number than others, supporting the notion that genetic factors may be involved in the susceptibility to large DA receptor responses to chronic haloperidol.