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 Ist 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 Ist, 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 IT 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 Ist 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. (C) 1998 Elsevier Science B.V.
机构:
Tokyo Univ Pharm & Life Sci, Dept Pharmacol, Hachioji, Tokyo 1920392, JapanTokyo Univ Pharm & Life Sci, Dept Pharmacol, Hachioji, Tokyo 1920392, Japan
Nagakura, A
Takeo, S
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机构:
Tokyo Univ Pharm & Life Sci, Dept Pharmacol, Hachioji, Tokyo 1920392, JapanTokyo Univ Pharm & Life Sci, Dept Pharmacol, Hachioji, Tokyo 1920392, Japan
Takeo, S
[J].
JAPANESE JOURNAL OF PHARMACOLOGY,
2002,
88
: 243P
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243P