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Stroke. 1995;26:1067-1071

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(Stroke. 1995;26:1067-1071.)
© 1995 American Heart Association, Inc.


Articles

Alterations of Brain Levels of Phosphoinositidase-C–Linked Gq{alpha}/G11{alpha} Proteins and Motor Function in Rats After Cardiac Arrest

Shyhwen P. Jaw, PhD; Duan D. Su, PharmD; Rae R. Matsumoto, PhD Daniel D. Truong, MD

From the Parkinson and Movement Disorders Laboratory, Department of Neurology, University of California, Irvine.

Background and Purpose Phosphoinositidase-C–linked Gq{alpha} and G11{alpha} 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{alpha} and G11{alpha} proteins are not known. Therefore, in the present studies, the effects of hypoxia-ischemia on Gq{alpha} and G11{alpha} 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{alpha} and G11{alpha} proteins were investigated by quantitative immunoblot analysis.

Results At 1, 2, 4, and 6 hours after resuscitation, Gq{alpha} and G11{alpha} 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-C–linked 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