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Correlations Between Na + ‐K + ATPase Activity and Acetylcholine Release in Rat Cortical Synaptosomes
Author(s) -
Meyer E. M.,
Cooper J. R.
Publication year - 1981
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1981.tb01616.x
Subject(s) - veratridine , ouabain , acetylcholine , chemistry , calcium , ionophore , tetrodotoxin , synaptosome , stimulation , sodium , choline , medicine , endocrinology , biophysics , biochemistry , biology , sodium channel , organic chemistry
[ 3 H]Acetylcholine efflux and Na + ‐K + ATPase ion pump activity were measured concomitantly in rat cortical synaptosomes. Ouabain (500 μM), strophanthidin (500 μM). and parachloromercuribenzene sulfonate (500 μM) each inhibited ouabain‐sensitive 86 Rb uptake and elevated [ 3 H]acetylcholine release independently of the external calcium concentration. Veratridine (10 μM), electrical field stimulation (60 V, 60 Hz, 5‐ms pulse duration), or the calcium ionophore A23187 (10μg/ml) also inhibited ouabain‐sensitive 86 Rb uptake and released [ 3 H]acetylcholine, but via a calcium‐dependent process. Veratridine‐induced [ 3 H]acetylcholine release and ion pump inhibition were correlated over a wide range of drug concentrations and both effects were blocked by pre‐treatment with tetrodotoxin (1 μM). The rate of [ 3 H]acetyl‐choline efflux from superfused synaptosomes was increased within 15 s of exposure to ouabain, strophanthidin, veratridine, A23187, or field stimulation, while ouabain‐sensitive 86 Rb uptake was significantly decreased within a similar interval. These results suggest that [ 3 H]acetylcholine release is due at least in part to inhibition of Na + ‐K + ATPase.