beta-Phenylethylamine reversal of chlorpromazine-induced activation of striatal tyrosine hydroxylase and catalepsy.
The ability of beta-phenylethylamine (PEA) to reverse (1) chlorpromazine-induced activation of striatal tyrosine hydroxylase, and (2) catalepsy produced by chlorpromazine, was examined. PEA, in a dose of 75 mg/kg, caused approximately 50% reduction in the degree of tyrosine hydroxylase stimulation produced by 20 mg/kg chlorpromazine. After 150 mg/kg PEA, complete reversal of tyrosine hydroxylase activation and partial reversal of catalepsy was observed. In these experiments, PEA was found to be about 10 times less potent than amphetamine and 25 times less potent than apomorphine. Thus, the ability of PEA to reverse the neurochemical and behavioral effects of striatal dopamine blockade is similar to known dopamine agonists.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002375:Catalepsy / Q000139:chemically induced / Q000503:physiopathology*; D002421:Caudate Nucleus / Q000187:drug effects / Q000502:physiology*; D002746:Chlorpromazine / Q000494:pharmacology*; D003913:Dextroamphetamine / Q000494:pharmacology; D006801:Humans; D008297:Male; D010627:Phenethylamines / Q000494:pharmacology*; D051381:Rats; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism*
D010627:Phenethylamines; C029261:phenethylamine; D014446:Tyrosine 3-Monooxygenase; D001058:Apomorphine; D003913:Dextroamphetamine; D002746:Chlorpromazine