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[Apoptosis in the repeated cerebral ischemia--behavioral & histochemical study]
K Iwasaki1, E H Chung, M Fujiwara
1Department of Physiology & Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Japan.
Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
|April 6, 1999
Summary
Repeated cerebral ischemia severely impairs spatial cognition in rats by causing cell death in the hippocampus. This cognitive decline and apoptosis are linked to non-NMDA receptor activity.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Context:
- Repeated cerebral ischemia causes significant spatial cognition deficits in rats, correlating with hippocampal CA1 pyramidal cell injury.
- Apoptosis, characterized by DNA fragmentation, is increasingly recognized in excitotoxic neuronal death.
Purpose:
- To investigate the roles of necrosis and apoptosis in cell death following repeated cerebral ischemia.
- To determine the involvement of specific receptor mechanisms in ischemia-induced neuronal damage and cognitive impairment.
Summary:
- Repeated cerebral ischemia (10 min x 2, 1 hr interval) induced lasting spatial cognition disruption and neuronal loss in the hippocampus CA1 area and frontal cortex.
- Apoptotic markers (DNA fragmentation, TUNEL-positive neurons) appeared later than neuronal death, suggesting a delayed apoptotic process.
- YM-90K, an AMPA/KA receptor antagonist, inhibited both spatial cognition deficits and apoptosis, while MK-801 did not.
Impact:
- Suggests that apoptotic cell death, mediated by non-NMDA receptors, occurs in the later reperfusion phase.
- Highlights a potential therapeutic target (non-NMDA receptors) for mitigating cognitive dysfunction after ischemic events.