ALTERATIONS OF BRAIN LEVELS OF PHOSPHOINOSITIDASE-C-LINKED G(Q-ALPHA)G(11-ALPHA) PROTEINS AND MOTOR FUNCTION IN RATS AFTER CARDIAC-ARREST/

Citation
Sp. Jaw et al., ALTERATIONS OF BRAIN LEVELS OF PHOSPHOINOSITIDASE-C-LINKED G(Q-ALPHA)G(11-ALPHA) PROTEINS AND MOTOR FUNCTION IN RATS AFTER CARDIAC-ARREST/, Stroke, 26(6), 1995, pp. 1067-1070
Citations number
34
Categorie Soggetti
Neurosciences,"Cardiac & Cardiovascular System","Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
26
Issue
6
Year of publication
1995
Pages
1067 - 1070
Database
ISI
SICI code
0039-2499(1995)26:6<1067:AOBLOP>2.0.ZU;2-0
Abstract
Background and Purpose Phosphoinositidase-C-linked G(q alpha) and G(11 alpha) proteins have only recently been characterized. Second messeng er systems are known to be affected by hypoxiaischemia. However, the e ffects of hypoxia-ischemia on the brain levels of G(q alpha) and G(11 alpha) proteins are not known. Therefore, in the present studies, the effects of hypoxia-ischemia on G(q alpha) and G(11 alpha) proteins in rats were investigated with quantitative immunoblot analysis. Methods Cardiac arrest was induced in male Sprague-Dawley rats by an intracard ial injection of KCl. Resuscitation began 10 minutes afterwards. At va rious time points after resuscitation, animals were killed and the cer ebral cortex, striatum, and cerebellum were dissected. Levels of G(q a lpha) and G(11 alpha) proteins were investigated by quantitative immun oblot analysis. Results At 1, 2, 4, and 6 hours after resuscitation, G (q alpha) and G(11 alpha) protein levels remained unaltered. However, a significant reduction of these proteins was seen in the cerebral cor tex and cerebellum of rats 3 and 14 days after cardiac arrest, with pa rtial recovery by an average of 60 days. In contrast, no significant c hange was detected in the striatum. Conclusions These observations ind icate that phosphoinositidase-C-linked signal transduction pathways ma y be attenuated after hypoxic-ischemic insults to the brain, and that this phenomenon, together with many other factors, may contribute to t he expression of motor dysfunction in rats after cardiac arrest.