Showing papers by "Angela Clow published in 1981"
TL;DR: The data suggest that at the critical 20- to 28-hour period after butaperazine administration, when most human acute dystonic reactions occur, normal or supersensitive cerebral dopamine receptors are exposed to an excessive synaptic release of dopamine, which may be responsible for the drug-induced dystonia.
Abstract: Oral administration of butaperazine (40 mg per kilogram) to rats increased dopamine turnover, as measured by elevation of striatal and mesolimbic concentrations of homovanillic acid and 3,4-dihydroxyphen-ylacetic acid, for 24 to 48 hours. Initially, this dose of butaperazine inhibited stereotyped behavior in response to subcutaneous administration of apomorphine, but this effect was reversed at 12 hours. Later, animals had normal or exaggerated responses to apomorphine. The data suggest that at the critical 20- to 28-hour period after butaperazine administration, when most human acute dystonic reactions occur, normal or supersensitive cerebral dopamine receptors are exposed to an excessive synaptic release of dopamine. This may be responsible for the drug-induced dystonia.
44 citations
TL;DR: Chronic neuroleptic administration to rats appears to alter specifically the number of cerebral dopamine receptors in the striatum and mesolimbic area, with a corresponding decrease in affinity for 3 H-spiperone binding.
19 citations
TL;DR: The disappearance of evidence of blockade of striatal dopamine receptors, which appeared to become supersensitive during a year's chronic treatment with either trifluoperazine or thioridazine, contrasts with the persistence of the effect of these drugs on serum prolactin levels.
13 citations