Open AccessCa 2+ Transport by Intact Synaptosomes: the Voltage‐Dependent Ca 2+ Channel and a Re‐evaluation of the Role of Sodium/Calcium Exchange
Author(s) -
AKERMAN Karl E. O.,
NICHOLLS David G.
Publication year - 1981
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1981.tb06364.x
Subject(s) - veratridine , verapamil , depolarization , chemistry , ouabain , efflux , biophysics , sodium , calcium , membrane potential , synaptosome , membrane , ion transporter , analytical chemistry (journal) , sodium channel , chromatography , biochemistry , biology , organic chemistry
The verapamil‐sensitive Ca 2+ channel in the synaptosomal plasma membrane is investigated. Verapamil is without effect on Ca 2+ uptake or steady‐state content in synaptosomes with a polarized plasma membrane, but completely inhibits the additional Ca 2+ uptake following plasma‐membrane depolarization by high [K + ], by veratridine plus ouabain or by high concentrations of the permeant cation tetraphenylphosphonium. Verapamilinsensitive Ca 2+ influx and steady‐state content are identical in polarized and depolarized synaptosomes, even though the Na + electrochemical potential is greatly decreased in the latter, indicating that Na + /Ca 2+ exchange is not a significant mechanism for Ca 2+ efflux under these conditions. A transient Na + ‐dependent Ca 2+ efflux can only be observed on addition of Na + to Na + ‐depleted, depolarized synaptosomes. While 0.2 mM verapamil decreases the rate of 86 Rb + efflux and 22 Na + entry during depolarization induced by veratridine plus ouabain, the final steady‐state Nat accumulation is not inhibited. Ca 2+ efflux from synaptosomes following mitochondrial depolarization does not occur by a verapamil‐sensitive pathway.