Phencyclidine and related compounds evoked [3H]dopamine release from rat mesencephalic cell cultures by a mechanism independent of the phencyclidine receptor, sigma binding site, or dopamine uptake site.
Canadian journal of physiology and pharmacology September 1, 1990 H Mount, P Boksa, I Chaudieu et al.
At high concentrations (≥100 μM), the drugs phencyclidine (PCP), TCP, and MK-801 triggered dopamine release from cultured rat mesencephalon cells. This release did not depend on calcium, was not blocked by tetrodotoxin, and was not stereoselective for certain drug enantiomers. A sigma ligand and a potassium channel blocker also induced release, but a dopamine uptake inhibitor did not affect spontaneous or TCP-evoked release. The findings suggest that PCP-like compounds cause dopamine release through a mechanism not involving PCP receptors, sigma sites, calcium or sodium channels, or the dopamine transporter, possibly by blocking voltage-regulated potassium channels.