Presynaptic dopamine receptors: insensitivity to kainic acid and the development of supersensitivity following chronic haloperidol.
The effects of kainic acid lesions and chronic haloperidol treatment on rat striatal dopaminergic presynaptic receptors were studied. Following the gamma-butyrolactone-induced inhibition of dopaminergic impulse flow, and after dopa decarboxylase inhibition, dopa accumulation and its reversal by dopamine agonists was measured in vivo. 3H-apomorphine (a dopamine receptor ligand with purported presynaptic specificity) was used for in vitro binding experiments. Presynaptic dopamine receptors, as assessed by both methods, were unaffected by intrastriatal kainic acid injection 5-6 days before sacrifice. Seven days after termination of chronic haloperidol treatment (28 days, 0.5 mg/kg/day s.c.) both an increased apomorphine response using the dopa accumulation method and an increase in 3H-apomorphine binding were observed, indicating the development of presynaptic dopamine receptor supersensitivity.
D015107:4-Butyrolactone / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000378:metabolism / Q000494:pharmacology; D003342:Corpus Striatum / Q000378:metabolism; D004295:Dihydroxyphenylalanine / Q000378:metabolism; D006220:Haloperidol / Q000008:administration & dosage / Q000494:pharmacology*; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D011759:Pyrrolidines / Q000494:pharmacology*; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects* / Q000378:metabolism
D011759:Pyrrolidines; D011954:Receptors, Dopamine; D004295:Dihydroxyphenylalanine; D006220:Haloperidol; D001058:Apomorphine; D015107:4-Butyrolactone; D007608:Kainic Acid