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(Stroke. 1995;26:1067-1071.)
© 1995 American Heart Association, Inc.
Articles |
/G11
Proteins and Motor Function in Rats After Cardiac Arrest
From the Parkinson and Movement Disorders Laboratory, Department of Neurology, University of California, Irvine.
Background and Purpose Phosphoinositidase-Clinked
Gq
and G11
proteins have only recently
been characterized. Second messenger systems are known to be affected
by hypoxia-ischemia. However, the effects of
hypoxia-ischemia on the brain levels of
Gq
and G11
proteins are not known.
Therefore, in the present studies, the effects of
hypoxia-ischemia on Gq
and
G11
proteins in rats were investigated with quantitative
immunoblot analysis.
Methods Cardiac arrest was induced in male
Sprague-Dawley rats by an intracardial injection of KCl.
Resuscitation began 10 minutes afterwards. At various time points after
resuscitation, animals were killed and the cerebral cortex, striatum,
and cerebellum were dissected. Levels of Gq
and
G11
proteins were investigated by quantitative
immunoblot analysis.
Results At 1, 2, 4, and 6 hours after resuscitation,
Gq
and G11
protein levels remained
unaltered. However, a significant reduction of these proteins was seen
in the cerebral cortex and cerebellum of rats 3 and 14 days after
cardiac arrest, with partial recovery by an average of 60 days. In
contrast, no significant change was detected in the striatum.
Conclusions These observations indicate that phosphoinositidase-Clinked signal transduction pathways may be attenuated after hypoxic-ischemic insults to the brain, and that this phenomenon, together with many other factors, may contribute to the expression of motor dysfunction in rats after cardiac arrest.
Key Words: hypoxia ischemia proteins rats myoclonus
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