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Journal of Neuroscience, Vol 9, 1701-1704, Copyright © 1989 by Society for Neuroscience
MK-801 prevents hypobaric-ischemic neuronal degeneration in infant rat brain
JW Olney, C Ikonomidou, JL Mosinger and G Frierdich
Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110.
Recent evidence implicates the endogenous excitatory amino acids, glutamate
(Glu) and aspartate, in hypoxic/ischemic neuronal degeneration. In a
preceding article (Ikonomidou et al., 1989) we described a new model for
studying hypoxic/ischemic neuronal degeneration in the infant rat brain
that entails unilateral common carotid artery ligation followed by exposure
to a partial vacuum for 75 min. Promising features of this model include a
low mortality rate and high incidence of acute brain damage disseminated
over numerous brain regions. In addition, there is a striking similarity
between the type of cytopathology characterizing this model of
hypoxic/ischemic neuronal degeneration and that which has been described in
infant animals treated with Glu. MK-801 is a powerful antagonist of the
N-methyl-D- aspartate (NMDA) receptor ionophore complex (a subtype of Glu
receptor). In the present study, after unilateral carotid artery ligation
was performed on 10-d-old rat pups, they were treated either with MK-801 (1
mg/kg i.p.) or saline 15 min before exposure to the hypobaric condition.
MK-801 exerted a strong neuroprotective effect without serious side
effects; the majority of saline control animals sustained severe brain
damage, whereas the majority of MK-801-treated pups had no brain damage.
These and other recent findings suggest that the NMDA receptor may play an
important role in hypoxic/ischemic neuronal degeneration in the immature
brain and provide hope that NMDA antagonists such as MK-801 may be
effective in preventing such degeneration.
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