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Modulation of Protein Kinase C Translocation by Excitatory and Inhibitory Amino Acids in Primary Cultures of Neurons
Author(s) -
Vaccarino Flora M.,
Liljequist Sture,
Tallman John F.
Publication year - 1991
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.1471-4159.1991.tb03765.x
Subject(s) - ampa receptor , protein kinase c , nmda receptor , excitatory postsynaptic potential , metabotropic glutamate receptor , inhibitory postsynaptic potential , long term depression , biology , biochemistry , metabotropic receptor , chemistry , glutamate receptor , receptor , microbiology and biotechnology , neuroscience , signal transduction
In primary cultures of neurons from rat cerebral cortex and neostriatum, excitatory amino acids stimulate the translocation of protein kinase C (PKC) from the cytoplasm to the membrane. In the presence of a physiological concentration of Mg 2+ in the extracellular medium, glutamate induces PKC translocation by binding to both TV‐methyl‐D‐aspartate (NMDA) and α‐amino‐3‐hydroxy‐5‐methylisoxazolepropionic acid (AMPA) excitatory amino acid receptors. Quisqualate translocates the enzyme by stimulating primarily AMPA receptors and possibly metabotropic receptors. NMDA receptor‐induced PKC translocation is sodium independent, whereas quisqualate receptor‐induced PKC translocation is sodium dependent; none of the agonists is active in the absence of calcium from the extracellular medium. Muscimol does not modify excitatory amino acid stimulation; however, blockade of γ‐aminobutyric acid A receptors by bicuculline greatly enhances glutamate‐induced PKC translocation. This enhancement is blocked by the NMDA receptor antagonist (+)‐5‐methyl‐10, 11‐dihydro‐ 5H ‐ dibenzo[ a , d ]cyclohepten‐5, 10‐imine hydrogen maleate (MK‐801) and by tetrodotoxin.