Potentiation of apomorphine action in rats by l-prolyl-l-leucyl-glycine amide.
Although the antiparkinsonian activity of 1-prolyl-l-leucyl-glycine amide (PLG=MIF-I) has been previously observed in several clinical trials, little is known of the mechanism of action of this tripeptide on the brain. Our study demonstrated potentiation of the action of apomorphine by PLG on the rotational behavior of mature rats which received unilateral 6-OHDA (16 microgram) lesions of the striatum as neonates. No change in tyrosine hydroxylase or dopa decarboxylase activities in rat striatal homogenates was found after addition of PLG (10(-8-10(-3) M). The results suggest that PLG modifies the dopamine receptor, making it more responsive to stimulation by the agonistic agent apomorphine and perhaps by the natural neurotransmitter dopamine.
D000818:Animals; D001058:Apomorphine / Q000037:antagonists & inhibitors*; D001522:Behavior, Animal / Q000187:drug effects*; D003342:Corpus Striatum / Q000187:drug effects; D003913:Dextroamphetamine / Q000037:antagonists & inhibitors; D004296:Dopa Decarboxylase / Q000378:metabolism; D004357:Drug Synergism; D005260:Female; D066298:In Vitro Techniques; D009075:MSH Release-Inhibiting Hormone / Q000494:pharmacology*; D008297:Male; D051381:Rats; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D009075:MSH Release-Inhibiting Hormone; D014446:Tyrosine 3-Monooxygenase; D004296:Dopa Decarboxylase; D001058:Apomorphine; D003913:Dextroamphetamine