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Neurotrophin‐3 (NT‐3) diminishes susceptibility of the oligodendroglial lineage to AMPA glutamate receptor‐mediated excitotoxicity
Author(s) -
Kavanaugh Bryan,
Beesley Jacqueline,
Itoh Takayuki,
Itoh Aki,
Grinspan Judith,
Pleasure David
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/1097-4547(20000615)60:6<725::aid-jnr4>3.0.co;2-v
Subject(s) - excitotoxicity , ampa receptor , glutamate receptor , neurotrophin , microbiology and biotechnology , tropomyosin receptor kinase c , biology , tropomyosin receptor kinase a , receptor , neuroscience , chemistry , biochemistry , growth factor , platelet derived growth factor receptor
Prior reports demonstrated that cells of the oligodendroglial lineage are susceptible to excitotoxic necrosis mediated by α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid glutamate receptors (AMPA‐GluR), and also showed that these cells express the high affinity neurotrophin receptors, TrkC and TrkA. We now report that: a) oligodendroglial progenitors (OP) and immature oligodendroglia are more vulnerable to AMPA‐GluR‐mediated excitotoxicity than are mature oligodendroglia; b) TrkC expression falls substantially during differentiation of cultured OP to mature oligodendroglia, whereas TrkA expression increases markedly; and c) neurotrophin‐3, and to a lesser extent, nerve growth factor, protect the oligodendroglial lineage against AMPA‐GluR‐mediated excitotoxicity. J. Neurosci. Res. 60:725–732, 2000. © 2000 Wiley‐Liss, Inc.