Modulation of Protein Kinase C Translocation by Excitatory and Inhibitory Amino Acids in Primary Cultures of Neurons

Modulation of Protein Kinase C Translocation by Excitatory and Inhibitory Amino Acids in Primary... 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 Mg2+ 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 acidA 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Modulation of Protein Kinase C Translocation by Excitatory and Inhibitory Amino Acids in Primary Cultures of Neurons

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Publisher
Wiley
Copyright
Copyright © 1991 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3042
eISSN
1471-4159
D.O.I.
10.1111/j.1471-4159.1991.tb03765.x
Publisher site
See Article on Publisher Site

Abstract

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 Mg2+ 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 acidA 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.

Journal

Journal of NeurochemistryWiley

Published: Aug 1, 1991

References

  • Synapse‐specific protein kinase C activation enhances maintenance of long‐term potentiation in rat hippocampus
    Lovinger, Lovinger; Routtenberg, Routtenberg
  • Translocation and activation of protein kinase C in striatal neurons in primary culture: relationship to phorbol dibutyrate actions on the inositol phosphate generating system and neurotransmitter release
    Weiss, Weiss; Ellis, Ellis; Hendtey, Hendtey; Lenox, Lenox

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