Open AccessPhencyclidine in low doses selectively blocks a presynaptic voltage-regulated potassium channel in rat brain.
Author(s) -
D K Bartschat,
M. P. Blaustein
Publication year - 1986
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.83.1.189
Subject(s) - phencyclidine , potassium channel , pharmacology , neuroscience , chemistry , neurotransmitter , neurotransmission , hallucinogen , biophysics , biology , receptor , biochemistry , central nervous system , nmda receptor
Phencylidine (PCP) is a major drug of abuse in the United States. It produces a toxic confusional psychosis in man. We show here that nanomolar to micromolar concentrations of PCP and behaviorally active congeners selectively block voltage-regulated noninactivating (or very slowly inactivating) presynaptic K channels in the brain. The rank order of potency for blockage of these K channels parallels both the relative ability of these agents to produce characteristic behavioral deficits in rats and their ability to displace [3H]PCP from its high-affinity binding sites in brain. In view of the enhanced voltage-gated Ca influx that would be expected to accompany blockage of presynaptic K channels, this mechanism could explain the excessive neurotransmitter release that is characteristic of PCP intoxication.