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Maitotoxin‐Evoked γ‐Aminobutyric Acid Release Is Due Not Only to the Opening of Calcium Channels
Author(s) -
Pin JeanPhilippe,
Yasumoto Takeshi,
Bockaert Joël
Publication year - 1988
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.1471-4159.1988.tb10597.x
Subject(s) - nipecotic acid , aminobutyric acid , tetrodotoxin , chemistry , endogeny , biophysics , calcium , nifedipine , gamma aminobutyric acid , liberation , biochemistry , neurotransmitter , receptor , biology , in vitro , organic chemistry
The effects of maitotoxin (MTX) on endogenous amino acid release were tested on highly purified striatal neurons differentiated in primary culture. MTX induced a large and concentration‐dependent release of γ‐aminobutyric acid (GABA). This effect was abolished when experiments were performed in the absence of external Ca 2+ , and restored when Ca 2+ ions were added after removing the MTX‐containing Ca 2+ ‐free solution. MTX‐induced amino acid release was not affected by 1 μ M nifedipine and only slightly inhibited by 1 m M Co 2+ . MTX also induced a massive accumulation of 45 Ca 2+ in the neurons which, in contrast to the MTX‐evoked GABA release, was totally blocked in the presence of 1 m M Co 2+ . Whereas 500 n M tetrodotoxin was without significant effect, MTX‐evoked GABA release was dependent on the presence of external Na + and sensitive to nipecotic acid, a GABA uptake inhibitor. It is concluded that, on striatal neurons, MTX induced Na + influx only in the presence of external Ca 2+ . The increase in cytoplasmic Na + ions then triggers the release of GABA.