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.
|Number of pages||4|
|State||Published - 1 Jan 1981|
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