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Barium‐Evoked Glutamate Release from Guinea‐Pig Cerebrocortical Synaptosomes
Author(s) -
McMahon H. T.,
Nicholls D. G.
Publication year - 1993
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.1471-4159.1993.tb03543.x
Subject(s) - exocytosis , biophysics , glutamate receptor , divalent , chemistry , synaptic vesicle , depolarization , kinetics , 4 aminopyridine , synaptosome , dissociation (chemistry) , calcium , calmodulin , guinea pig , biochemistry , membrane , vesicle , biology , endocrinology , receptor , potassium channel , physics , organic chemistry , quantum mechanics
Ba 2+ has multiple effects on presynaptic terminals. The ion inhibits the K + channels responsible for stabilizing the plasma membrane potential in the same way as previously reported for dendrotoxin and 4‐aminopyridine. Secondly, the ion can substitute fully for Ca 2+ in supporting KCl‐evoked release of glutamate from guinea‐pig cerebrocortical synaptosomes. In the latter case, the kinetics of glutamate release in the presence of saturating Ca 2+ or Ba 2+ are essentially identical. Substantially lower external concentrations of Ba 2+ are required to achieve the same release kinetics as with Ca 2+ . The average internal free Ba 2+ concentration attained during KCl depolarization is some 10‐fold higher than that for Ca 2+ . However, because the fura‐2 signal reflects predominantly the overflow of divalent cation after dissociation from the release trigger, it is not the valid parameter to compare effectiveness of the cations in triggering glutamate exocytosis. In view of the established inability of Ba 2+ to interact with calmodulin, these results are discussed in relation to theories in which Ca 2+ /calmodulin‐dependent protein kinase‐mediated phosphorylation is a prerequisite for synaptic vesicle exocytosis.