In the primary cultures of embryonic mesencephalic neurons specific binding sites for dopamine uptake blockers were detectable in the cytosol but not in synaptosomal membranes. Pharmacological studies showed that the cytosolic binding sites were not functionally associated with the membrane located dopamine transporter but were a piperazine-acceptor site. Studies on the regulation of dopamine release showed that N-type calcium channel blockers selectively blocked K+-depolarization evoked dopamine release. N- type channel bockers inhibited the rise in specific calcium pools located in neurites and thereby provided a calcium-dependent constraint on dopamine release. In addition, our data provided evidence that glutamate receptor stimulation at a post-synaptic location leads to nitric oxide formation serving as a diffusable signal operative in dopamine release from axonal terminals.
