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Magnesium Ions Inhibit the Stimulation of Inositol Phospholipid Hydrolysis by Endogenous Excitatory Amino Acids in Primary Cultures of Cerebellar Granule Cells
Author(s) -
Nicoletti F.,
Wroblewski J. T.,
Costa E.
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.tb05611.x
Subject(s) - veratridine , kainate receptor , nmda receptor , glutamate receptor , quisqualic acid , excitatory postsynaptic potential , chemistry , biochemistry , stimulation , depolarization , biology , receptor , biophysics , kainic acid , endocrinology , ampa receptor , sodium , sodium channel , organic chemistry
Omission of Mg 2+ from the incubation buffer results in a six‐ to eightfold increase in [ 3 H]inositol‐1‐phosphate ([ 3 H]Ins‐1‐P) accumulation in primary cultures of cerebellar granule cells at 7–9 days in vitro. This increase is reversed by low concentrations of 2‐amino‐5‐phosphonovalerate (APV), a result indicating that the absence of Mg 2+ facilitates the activation of a specific receptor by the endogenous excitatory amino acids (presumably l‐glutamate and l‐aspartate) released from the granule cells. The absence of Mg 2+ also potentiates the action of exogenously applied N‐ methyl‐d‐aspartate (NMDA), l‐glutamate, l‐aspartate, and kainate. In contrast, the action of quisqualate is virtually unaffected by Mg 2+ and is resistant to APV inhibition. Addition of the depolarizing agent veratridine enhances the accumulation of [ 3 H]Ins‐1‐P also in Mg 2+ ‐containing buffer. The action of veratridine is antagonized by APV, a result suggesting that, under depolarized conditions, the NMDA receptor can be activated by the endogenously released excitatory amino acids, despite the presence of Mg 2+ . Accordingly, in the presence of Mg 2+ , veratridine potentiates the action of exogenously applied NMDA but does not facilitate the action of quisqualate.