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Microsphere embolism-induced changes in noradrenaline release in the cerebral cortex in rats
H Hayashi1, K Sato, Y Kuruhara
1Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Tokyo, Japan.
Brain Research
|April 18, 1998
Summary
Microsphere embolism in rats impairs noradrenaline release and alters synaptic vesicle structure. This suggests a failure in synapsin I phosphorylation contributes to the observed neurological changes.
Area of Science:
- Neuroscience
- Pathophysiology
- Biochemistry
Background:
- Microsphere embolism is a model for studying cerebrovascular events.
- Understanding changes in neurotransmitter release and neuronal ultrastructure is crucial for neurological research.
Purpose of the Study:
- To investigate pathophysiological changes in noradrenaline release.
- To examine synapsin I phosphorylation and nerve terminal ultrastructure after microsphere embolism.
- To elucidate the mechanisms underlying neurological deficits.
Main Methods:
- Microdialysis was used to measure K+-stimulated noradrenaline release in rat cerebral cortex.
- Synaptosomes were isolated to analyze calmodulin, synapsin I, and calcium/calmodulin-dependent protein kinase II levels and phosphorylation.
- Electron microscopy examined the ultrastructure of cerebrocortical nerve terminals.
Main Results:
- Noradrenaline release decreased significantly on days 3 and 7 post-embolism.
- Levels of calcium/calmodulin-dependent protein kinase II and synapsin I were reduced.
- Electron microscopy revealed aggregation of synaptic vesicles on days 3 and 7.
Conclusions:
- Microsphere embolism disrupts noradrenaline release, potentially due to impaired synapsin I phosphorylation.
- Synaptic vesicle aggregation may play a role in the pathogenesis of microsphere embolism.
- These findings provide insights into the neurobiological consequences of cerebrovascular events.