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Microsphere embolism-induced changes in noradrenaline release in the cerebral cortex in rats.

作者信息

Hayashi H, Sato K, Kuruhara Y, Takeo S

机构信息

Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Tokyo, Japan.

出版信息

Brain Res. 1998 Feb 9;783(2):241-8. doi: 10.1016/s0006-8993(97)01338-3.

Abstract

The present study was undertaken to elucidate pathophysiological changes in noradrenaline release, phosphorylation of synapsin I and ultrastructure of the cerebrocortical nerve terminals following microsphere embolism in rats. In the microdialysis study, K+-stimulated noradrenaline release in the cerebral cortex was not altered on the 1st day but markedly decreased on the 3rd and 7th days after the embolism. Synaptosomes were isolated from the cerebral cortex of the operated animals on the 1st, 3rd and 7th days after the embolism. The level of calmodulin and the phosphorylation of synapsin I in the synaptosomes were not altered up to the 7th day, but the levels of calcium/calmodulin-dependent protein kinase II and synapsin I in the synaptosomes were significantly decreased by microsphere embolism. Electron microscopic study showed no appreciable changes in the structure of the synaptosomes on the 1st day, but a large number of clumps of synaptic vesicles were observed on the 3rd and 7th days after the embolism. These results suggest that microsphere embolism-induced changes in noradrenaline release from nerve terminals are due to a failure in the process following phosphorylation of synapsin I. Aggregation of synaptic vesicles in nerve terminals may contribute to the pathogenesis of microsphere embolism.

摘要

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