Dopamine autoreceptors modulate dopamine release from the prefrontal cortex.
Electrical stimulation (at 0.3, 1, or 10 Hz, 120 pulses each) produced a calcium-dependent overflow of radioactivity from slices of the rabbit prefrontal cortex preloaded with [3H]3,4-dihydroxyphenylethylamine ([3H]DA, [3H]dopamine) in the presence of desipramine. Flat frequency-release curves were observed. Apomorphine and LY-171555 inhibited in a concentration-dependent fashion the evoked overflow of DA, an effect antagonized by haloperidol. Stimulation frequencies comparable to normal firing rates of mesocortical neurons (10 Hz) drastically reduced apomorphine-induced inhibition of DA overflow. Haloperidol produced greater facilitation of DA overflow at 10 than at 1 Hz. Nomifensine, a neuronal uptake inhibitor, enhanced DA overflow. These results indicate that mesocortical DA neurons projecting to the prefrontal cortex have release modulatory autoreceptors of the D2 subtype.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D003891:Desipramine / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism*; D004558:Electric Stimulation; D004873:Ergolines / Q000494:pharmacology; D005260:Female; D005625:Frontal Lobe / Q000187:drug effects / Q000378:metabolism*; D006220:Haloperidol / Q000494:pharmacology; D008297:Male; D009627:Nomifensine / Q000494:pharmacology; D019257:Quinpirole; D011817:Rabbits; D011954:Receptors, Dopamine / Q000502:physiology*
D004873:Ergolines; D011954:Receptors, Dopamine; D009627:Nomifensine; D019257:Quinpirole; D006220:Haloperidol; D001058:Apomorphine; D002118:Calcium; D003891:Desipramine; D004298:Dopamine