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Journal of Neuroscience, Vol 10, 311-316, Copyright © 1990 by Society for Neuroscience
Hypothermia but not the N-methyl-D-aspartate antagonist, MK-801, attenuates neuronal damage in gerbils subjected to transient global ischemia
A Buchan and WA Pulsinelli
Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021.
Several laboratories have reported a significant reduction of ischemia-
induced injury to hippocampal neurons in rodents treated with competitive
and noncompetitive N-methyl-D-aspartate (NMDA) receptor- channel
antagonists. This study examined the effects of the noncompetitive
antagonist (+)-5-methyl-10,11-dihydro-5H-
dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) in Mongolian gerbils
subjected to 5 min of bilateral carotid artery occlusion. In adult female
gerbils, single doses of MK-801 injected 1 hr prior to ischemia
significantly (p less than 0.01) reduced damage to CA1 hippocampal neurons.
However, the drug rendered the postischemic animals comatose and
hypothermic for several hours compared with the saline-treated animals. In
subsequent experiments, animals pretreated with MK-801 and maintained
normothermic during and after forebrain ischemia demonstrated no
amelioration of hippocampal damage. Gerbils not treated with MK-801, but
kept hypothermic in the postischemic period to approximately the same
degree (34.5 degrees C) and duration (8 hr) as was induced by MK-801
therapy showed significant (p less than 0.01) protection of CA1 neurons
against ischemia. The neuroprotective activity of MK-801 against transient
global ischemia appears to be largely a consequence of postischemic
hypothermia rather than a direct action on NMDA receptor-channels.
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