PMID- 7520088
OWN - NLM
STAT- MEDLINE
DCOM- 19940915
LR  - 20161123
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 38
IP  - 1
DP  - 1994 May 1
TI  - Depolarizing agents and tumor necrosis factor-alpha modulate protein 
      phosphorylation in oligodendrocytes.
PG  - 91-100
AB  - 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 the phosphorylation states of their proteins and perhaps affect 
      myelin maintenance, contributing to demyelination.
FAU - Soliven, B
AU  - Soliven B
AD  - Department of Neurology, University of Chicago, Illinois 60637.
FAU - Takeda, M
AU  - Takeda M
FAU - Szuchet, S
AU  - Szuchet S
LA  - eng
GR  - P01 NS24575/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Myelin Basic Protein)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neuromuscular Depolarizing Agents)
RN  - 0 (Potassium Channels)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
RN  - EC 3.1.4.- (2',3'-Cyclic-Nucleotide Phosphodiesterases)
RN  - EC 3.1.4.- (Phosphoric Diester Hydrolases)
RN  - EC 3.1.4.37 (2',3'-Cyclic Nucleotide 3'-Phosphodiesterase)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase
MH  - 2',3'-Cyclic-Nucleotide Phosphodiesterases/antagonists & inhibitors
MH  - Animals
MH  - Cells, Cultured
MH  - Membrane Potentials/drug effects
MH  - Myelin Basic Protein/biosynthesis
MH  - Nerve Tissue Proteins/*metabolism
MH  - Neuromuscular Depolarizing Agents/*pharmacology
MH  - Oligodendroglia/drug effects/*metabolism
MH  - *Phosphoric Diester Hydrolases
MH  - Phosphoric Monoester Hydrolases/antagonists & inhibitors
MH  - Phosphorylation
MH  - Potassium/pharmacology
MH  - Potassium Channels/drug effects/metabolism
MH  - Protein Kinase C/metabolism
MH  - Sheep
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1994/05/01 00:00
MHDA- 1994/05/01 00:01
CRDT- 1994/05/01 00:00
PHST- 1994/05/01 00:00 [pubmed]
PHST- 1994/05/01 00:01 [medline]
PHST- 1994/05/01 00:00 [entrez]
AID - 10.1002/jnr.490380112 [doi]
PST - ppublish
SO  - J Neurosci Res. 1994 May 1;38(1):91-100. doi: 10.1002/jnr.490380112.