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J Neurophysiol 85: 900-911, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 85 No. 2 February 2001, pp. 900-911
Copyright ©2001 by the American Physiological Society

Axonal L-Type Ca2+ Channels and Anoxic Injury in Rat CNS White Matter

Angus M. Brown,1 Ruth E. Westenbroek,2 William A. Catterall,2 and Bruce R. Ransom1

 1Department of Neurology and  2Department of Pharmacology, University of Washington School of Medicine, Seattle, Washington 98195

Brown, Angus M., Ruth E. Westenbroek, William A. Catterall, and Bruce R. Ransom. Axonal L-Type Ca2+ Channels and Anoxic Injury in Rat CNS White Matter. J. Neurophysiol. 85: 900-911, 2001. We studied the magnitude and route(s) of Ca2+ flux from extra- to intracellular compartments during anoxia in adult rat optic nerve (RON), a central white matter tract, using Ca2+-sensitive microelectrodes to monitor extracellular [Ca2+] ([Ca2+]o). One hour of anoxia caused a rapid loss of the stimulus-evoked compound action potential (CAP), which partially recovered following re-oxygenation, indicating that irreversible injury had occurred. After an initial increase caused by extracellular space shrinkage, anoxia produced a sustained decrease of 0.42 mM (29%) in [Ca2+]o. We quantified the [Ca2+]o decrease as the area below baseline [Ca2+]o during anoxia and used this as a qualitative index of suspected Ca2+ influx. The degree of RON injury was predicted by the amount of Ca2+ leaving the extracellular space. Bepridil, 0 Na+ artificial cerebrospinal fluid or tetrodotoxin reduced suspected Ca2+ influx during anoxia implicating reversal of the Na+-Ca2+ exchanger as a route of Ca2+ influx. Diltiazem reduced suspected Ca2+ influx during anoxia, suggesting that Ca2+ influx via L-type Ca2+ channels is a route of toxic Ca2+ influx into axons during anoxia. Immunocytochemical staining was used to demonstrate and localize high-threshold Ca2+ channels. Only alpha 1C and alpha 1D subunits were detected, indicating that only L-type Ca2+ channels were present. Double labeling with anti-neurofilament antibodies or anti-glial fibrillary acidic protein antibodies, localized L-type Ca2+ channels to axons and astrocytes.




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