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Kainic Acid Inhibits the Synaptosomal Plasma Membrane Glutamate Carrier and Allows Glutamate Leakage from the Cytoplasm but Does Not Affect Glutamate Exocytosis
Author(s) -
Pocock Jennifer M.,
Murphie Helen M.,
Nicholls David G.
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.tb02977.x
Subject(s) - kainate receptor , glutamate receptor , biophysics , kainic acid , endogeny , biochemistry , chemistry , glutamic acid , exocytosis , biology , amino acid , membrane , ampa receptor , receptor
Kainate inhibits the exchange of d‐aspartate into guinea‐pig cerebrocortical synaptosomes. Kainate inhibits the Ca 2+ ‐independent efflux of endogenous glutamate in the presence of a trapping system for the released amino acid but potentiates a Ca 2+ ‐independent net efflux of endogenous and labelled glutamate and aspartate in the ab‐sence of the trap. Dihydrokainate has a similar effect. No discrepancy is seen between the release of endogenous and exogenously accumulated amino acid. These results are consistent with the presence of a slow leak of glutamate or aspartate from the cytoplasm independent of the kainate‐sensitive Na + ‐cotransport pathway. In the presence of the trap, glutamate effluxes by both pathways, whereas in the absence of the trap, the Na + ‐cotransport pathway opposes the leak. Neither in the presence or absence of the glutamate trap does kainate induce, inhibit, or otherwise affect the Ca 2+ ‐dependent release of endogenous glutamate. The results enable many of the apparent complexities in the presynaptic actions of kainate to be resolved.