Depolarizing agents and tumor necrosis factor-alpha modulate protein phosphorylation in oligodendrocytes

Journal of Neuroscience Research
B SolivenS Szuchet

Abstract

Membrane depolarization and changes in ionic fluxes have been implicated in the signaling mechanisms between neurons and glial cells. We report here that K(+)-induced depolarization of cultured ovine oligodendrocytes (OLGs) decreases the phosphorylation of myelin basic protein (MBP) and 2'3'-cyclic nucleotide phosphohydrolase (CNPase). Membrane depolarization and decrease in phosphorylation of MBP and CNPase can also be elicited by inhibition of the inward rectifier with Ba2+ but not by inhibition of outward K+ channels with 4-aminopyridine or tetraethylammonium. These findings demonstrate that modulation of K+ currents can influence phosphorylation states of OLG proteins. Tumor necrosis factor-alpha (TNF-alpha), an immune peptide implicated in autoimmune demyelinating diseases, also inhibits the phosphorylation of these proteins. In contrast to elevated [K+]o, TNF-alpha does not decrease the stimulatory effect of protein kinase C activators or phosphatase inhibitors on MBP and CNPase phosphorylation, suggesting that depolarizing agents and TNF-alpha act via distinct mechanisms. We postulate that the presence of elevated extracellular K+ and/or cytokines under certain pathological conditions can perturb OLG function by altering...Continue Reading

References

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Citations

Jun 1, 1995·International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience·B Soliven, S Szuchet
Jul 23, 2003·Neuroscience Research·Shin HisaharaMasayuki Miura
Jan 13, 2000·Neuropathology and Applied Neurobiology·J E Merrill, N J Scolding
Dec 23, 2006·Journal of Neurotrauma·Judith M LytleJean R Wrathall
Oct 12, 2001·Glia·T BennN Scolding
Feb 13, 2013·Journal of Neurochemistry·George Harauz, Joan M Boggs

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