| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Department of Neurology, Yale University School of Medicine, New Haven, and PVA/EPVA Neuroscience Research Center, Veterans Administration Medical Center, West Haven, CT.
Gray and white matter of the mammalian CNS are both damaged by anoxia. Anoxic injury in gray matter is mediated in part by excessive accumulation of excitotoxins like glutamate. Drugs such as ketamine, a dissociative anesthetic known to block glutamate (NMDA) receptors, reduce hypoxic neuronal injury in gray matter. In this study we used the isolated rat optic nerve preparation to determine if ketamine influences recovery after anoxia in a nonsynaptic system, ie, CNS white matter. Optic nerves from adult rats were exposed to a standard 60-minute period of anoxia. Ketamine (1 mM) improved recovery of the compound action potential (CAP) after anoxia. Since glutamate and aspartate (up to 10 mM) had no effect on CAP amplitude in the optic nerve, the effect of ketamine is probably not mediated by NMDA receptor blockade. These observations indicate that ketamine is able to protect CNS white matter, as well as gray matter, from anoxic injury.
Address correspondence and reprint requests to Dr. Bruce R. Ransom, Department of Neurology, LCI 707, Yale Medical School, 333 Cedar Street, New Haven, CT06510
Supported in part by grants from the National Institutes of Health, and by the Medical Research Service, Veterans Administration. P.K.D. was supported, in part, by a grant from the Blinded Veterans Associatiobt.
Received January 15, 1990. Accepted for publication in final form February 28, 1990.
This article has been cited by other articles:
|
|
 |
|
  S. Baltan, E. F. Besancon, B. Mbow, Z. Ye, M. A. Hamner, and B. R. Ransom White Matter Vulnerability to Ischemic Injury Increases with Age Because of Enhanced Excitotoxicity J. Neurosci., February 6, 2008; 28(6): 1479 - 1489. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. M. Frohman, M. Filippi, O. Stuve, S. G. Waxman, J. Corboy, J. T. Phillips, C. Lucchinetti, J. Wilken, N. Karandikar, B. Hemmer, et al. Characterizing the Mechanisms of Progression in Multiple Sclerosis: Evidence and New Hypotheses for Future Directions Arch Neurol, September 1, 2005; 62(9): 1345 - 1356. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Brown, R. E. Westenbroek, W. A. Catterall, and B. R. Ransom Axonal L-Type Ca2+ Channels and Anoxic Injury in Rat CNS White Matter J Neurophysiol, February 1, 2001; 85(2): 900 - 911. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W.-R. Schabitz, F. Li, M. Fisher, and P. H. Chan The N-Methyl-D-Aspartate Antagonist CNS 1102 Protects Cerebral Gray and White Matter From Ischemic Injury Following Temporary Focal Ischemia in Rats Editorial Comment Stroke, July 1, 2000; 31(7): 1709 - 1714. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. P. Blaustein and W. J. Lederer Sodium/Calcium Exchange: Its Physiological Implications Physiol Rev, July 1, 1999; 79(3): 763 - 854. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. D. Teng and J. R. Wrathall Local Blockade of Sodium Channels by Tetrodotoxin Ameliorates Tissue Loss and Long-Term Functional Deficits Resulting from Experimental Spinal Cord Injury J. Neurosci., June 1, 1997; 17(11): 4359 - 4366. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Li, G. A. R. Mealing, P. Morley, and P. K. Stys Novel Injury Mechanism in Anoxia and Trauma of Spinal Cord White Matter: Glutamate Release via Reverse Na+-dependent Glutamate Transport J. Neurosci., July 15, 1999; 19(14): RC16 - RC16. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
