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The Effect of Antibodies to Gangliosides on Ca 2+ Channel‐Linked Release of γ‐Aminobutyric Acid in Rat Brain Slices
Author(s) -
Frieder B.,
Rapport M. M.
Publication year - 1987
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.1471-4159.1987.tb05625.x
Subject(s) - depolarization , tetrodotoxin , ionophore , ganglioside , aminobutyric acid , chemistry , biophysics , gamma aminobutyric acid , biochemistry , biology , receptor , membrane
Antibodies to G m1 ganglioside enhance the release of γ‐aminobutyric acid (GABA) from rat brain slices induced by depolarization with either 40 m M K + or 200 μ M veratrine. Three new observations are now reported, (a) GABA release induced by the Ca 2+ ionophore A23187 was not affected by these antibodies. Because this Ca 2+ ionophore causes transmitter release by bypassing depolarization‐induced opening of Ca 2+ channels, this result suggests that gangliosides participate either in the functioning of such Ca 2+ channels or in the Na + channels involved in depolarization, (b) The enhancement (by antibodies to G M1 ganglioside) of GABA release induced by high K + levels occurred in the presence of tetrodotoxin (0.01 μ M ). (c) GABA release induced by veratrine in the absence of Ca 2+ was not affected by the antibodies. These latter two observations indicate that Na + channels are not involved in the action of the antibodies. We conclude that this evidence points to the participation of gangliosides in Ca 2+ channel functions involved in GABA release in rat brain slices.