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Microsphere embolism-induced changes in presynaptic function of the cerebral cortex in rats
H Hayashi1, N Takagi, N Kamimoto
1Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Hachioji, Japan.
Brain Research
|October 21, 1996
Summary
Microsphere embolism in rats impairs cerebrocortical nerve terminal function, decreasing calcium influx and noradrenaline release/uptake. P-type calcium channels are predominant in rat brain cortex.
Area of Science:
- Neuroscience
- Pharmacology
- Pathophysiology
Background:
- Cortical presynaptic function is crucial for neurotransmission.
- Microsphere embolism can induce cerebral ischemia and affect neuronal function.
- Understanding changes in calcium influx and noradrenaline pathways is vital for neurological research.
Purpose of the Study:
- To investigate pathophysiological changes in cortical presynaptic function after microsphere embolism.
- To characterize voltage-dependent calcium channels involved in K(+)-stimulated calcium influx.
- To assess the impact of embolism on noradrenaline release and uptake.
Main Methods:
- Microsphere embolism model in rats.
- Pharmacological characterization of calcium channels using specific blockers (L-type, N-type, P-type).
- Measurement of K(+)-stimulated calcium influx, noradrenaline release, and uptake in cortical synaptosomes.
Main Results:
- K(+)-stimulated calcium influx in normal rat synaptosomes was predominantly inhibited by P-type channel blockers.
- Microsphere embolism decreased calcium influx, noradrenaline release, and noradrenaline uptake in cortical nerve terminals.
- The percentage of noradrenaline release remained unaltered, suggesting uptake dysfunction.
Conclusions:
- P-type calcium channels play a predominant role in rat cerebrocortical nerve terminals.
- Microsphere embolism leads to decreased calcium influx, noradrenaline release, and uptake.
- Reduced noradrenaline release is likely attributed to impaired noradrenaline uptake activity post-embolism.