Functional increase in striatal dopaminergic activity following continuous long-term treatment with trifluoperazine.
Acute administration of trifluoperazine (2-10 mg/kg i.p.) caused a dose-dependent increase in potassium (K+)-evoked release of [3H]acetylcholine from striatal slices, but was without effect on K+-evoked release of [3H]glutamate. K+-evoked [3H]acetylcholine release was not different in striatal tissue from rats receiving 1 year's continuous administration of trifluoperazine (4.5-5.1 mg/kg/day) compared to age-matched control animals. However, K+-evoked striatal [3H]glutamate release was decreased in tissue from chronically trifluoperazine-treated animals compared to age-matched controls. The reversal of the acute action of trifluoperazine on striatal [3H]acetylcholine and the decrease of [3H]glutamate release on chronic administration is consistent with adaptive changes in striatal dopamine transmission during long-term neuroleptic treatment.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects*; D004298:Dopamine / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D008297:Male; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects; D014268:Trifluoperazine / Q000494:pharmacology*
D005971:Glutamates; D011954:Receptors, Dopamine; D014268:Trifluoperazine; D018698:Glutamic Acid; D000109:Acetylcholine; D011188:Potassium; D004298:Dopamine