期刊
NEUROBIOLOGY OF DISEASE
卷 25, 期 2, 页码 284-290出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2006.09.011
关键词
glutamate; AMPA/kainate; NMDA; calpain; axon; excitotoxicity; ischemia; oxygen-glucose deprivation; white matter
资金
- NINDS NIH HHS [NS32636, NS36265, R01 NS036265, P01 NS032636, P30 NS057105] Funding Source: Medline
Axonal injury in white matter is an important consequence of many acute neurological diseases including ischemia. A role for glutamate-mediated excitotoxicity is suggested by observations from in vitro and in situ models that AMPA/kainate blockers can reduce axonal injury. We assessed axonal vulnerability in primary murine neuronal cultures, with axons isolated from their cell bodies using a compartmented chamber design. Transient removal of oxygen and glucose in the axon compartment resulted in irreversible loss of axon length and neurofilament labeling. This injury was not prevented by addition of ionotropic glutamate receptor blockers and could not be reproduced by glutamate receptor agonists. However, hypoxic injury was prevented by blockade of voltage-gated sodium channels, inhibition of calpain and removal of extracellular calcium. These results suggest that isolated, unmyelinated axons are vulnerable to hypoxic injury which is mediated by influx of sodium and calcium but is independent of glutamate receptor activation. (c) 2006 Elsevier Inc. All rights reserved.
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