NDLI: Protein Kinase C Activation Attenuates N-Methyl-d-Aspartate-Induced Increases in Intracellular Calcium in Cerebellar Granule Cells

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Protein Kinase C Activation Attenuates N-Methyl-d-Aspartate-Induced Increases in Intracellular Calcium in Cerebellar Granule Cells

Content Provider	Scilit
Author	Snell, Lawrence D. Lorio, Karen R. Tabakoff, Boris Hoffman, Paula L.
Copyright Year	2008
Description	Journal: Journal of Neurochemistry Activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor increases levels of intracellular calcium and can lead to stimulation of protein kinase C activity. Several reports have demonstrated that stimulation of protein kinase C can, in turn, increase electrophysiological responses to NMDA in certain cells or in oocytes expressing certain NMDA receptor subunits. In the present study, the effects of protein kinase C activation on NMDA receptor-mediated increases in intracellular Ca2+ level were investigated in primary cultures of rat cerebellar granule cells using fura-2 fluorescence spectroscopy. Pretreatment of the cells with the protein kinase C activator phorbol 12-myristate 13-acetate (PMA), but not the inactive analogue 4 alpha-phorbol 12-myristate 13-acetate, inhibited NMDA-induced increases in intracellular Ca2+ levels. Coincubation of cells with PMA and the kinase inhibitor staurosporine or calphostin C blocked the PMA effect. The potency of NMDA was reduced twofold, and the potency of the NMDA receptor co-agonist, glycine, to enhance the response to NMDA was decreased fourfold by pretreatment of cells with PMA. The effect on glycine was mimicked by pretreatment with okadaic acid, a protein phosphatase inhibitor. PMA treatment did not significantly alter Mg2+ inhibition of the NMDA response but decreased the potency of the competitive antagonist CGS-19755. These data suggest that, in cerebellar granule cells, the function of the NMDA receptor may be subject to feed-back inhibition by protein kinase C stimulation. Under physiological conditions, this inhibition may result from a decreased effectiveness of the endogenous co-agonists, glutamate and glycine.
Related Links	http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1994.62051783.x/pdf
Ending Page	1789
Page Count	7
Starting Page	1783
e-ISSN	14714159
DOI	10.1046/j.1471-4159.1994.62051783.x
Journal	Journal of Neurochemistry
Issue Number	5
Volume Number	62
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2008-06-28
Access Restriction	Open
Subject Keyword	Journal: Journal of Neurochemistry Biochemistry and Molecular Biology Protein Kinase Co Agonist Induced Increases
Content Type	Text
Resource Type	Article

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