Journal
NEUROBIOLOGY OF DISEASE
Volume 9, Issue 2, Pages 234-243Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/nbdi.2001.0457
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Oligodendrocytes are vulnerable to excitotoxic insults mediated by AMPA receptors and by low and high affinity kainate receptors, a feature that is dependent on Ca2+ influx. In the current study, we have analyzed the intracellular concentration of calcium [Ca2+](i) as well as the entry routes of this cation, upon activation of these receptors. Selective activation of either receptor type resulted in a substantial increase (up to fivefold) of [Ca2+](i), an effect which was totally abolished by the non-NMDA receptor antagonist CNOX or by removing Ca2+ from the culture medium. Blockade of voltage-gated Ca2+ channels with La3+ or nifedipine, reduced the amplitude of the Ca2+ current triggered by AMPA receptor activation by similar to65%, but not that initiated by low and high affinity kainate receptors. In contrast, KB-R7943, an inhibitor of the plasma membrane Na+-Ca2+ exchanger, solely attenuated the rise in [Ca2+] by similar to25% due to activation of low affinity kainate receptors. However, oligodendroglial death by glutamate receptor overactivation was largely unaffected in the presence of La3+ or KB-R7943. These findings indicate that Ca2+ influx via AMPA and kainate receptors alone is sufficient to initiate cell death in oligodendrocytes, which does not require the entry of calcium via other routes such as voltage-activated calcium channels or the plasma membrane Na+-Ca2+ exchanger. (C) 2002 Elsevier Science (USA).
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