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The Na + ,K + ‐ATPase: A Plausible Trigger for Voltage‐Independent Release of Cytoplasmic Neurotransmitters
Author(s) -
O'Fallon James V.,
Brosemer Ronald W.,
Harding Joseph W.
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.tb01604.x
Subject(s) - ouabain , depolarization , biophysics , potassium , acetylcholine , chemistry , cytoplasm , atpase , biochemistry , sodium , biology , endocrinology , enzyme , organic chemistry
A comparison was made between the releasability of eight neurotransmitters from eight regions of mouse brain in response to either 60 μM‐K + or 20 μM‐ouabain, a specific inhibitor of the Na + , K + ‐ATPase. With few exceptions, all transmitters were released by either or both agents from each brain region examined. Potassium was superior in releasing the biogenic amines and acetylcholine, while the putative amino acid transmitters were generally releasable by both agents. Measurements of tissue depolarization using [ 3 H]‐tetraphenylphosphonium uptake indicated that 60 μM‐K + is capable of depolarizing brain tissue above the threshold necessary for initiating an action potential, but 20μM‐ouabain is not. The pattern of release by ouabain coupled with its failure to depolarize brain tissue at 20μM suggests that inhibition of the Na + ,K + ‐ATPase is capable of releasing cytoplasmic neurotransmitters in a voltage‐independent manner.