Stroke · 1995
Alterations of brain levels of phosphoinositidase-C-linked Gq alpha/G11 alpha proteins and motor function in rats after cardiac arrest.
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Jaw S P, Su D D, Matsumoto R R, Truong D D
Аннотация
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.
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.