| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1987: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1986: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
Brier transient forbrain ischemia in to Mongolian gearbil produces a selective neuronal damage in the hippocampus. Immeciately follwing ishemia, prentobarbvtal,diazapem, or nizotenone were given in gerbils. The neuronal density in the CA1 sector showed a significant inforease in the treated goups. when froug administration was delayed fro longer than 15 minutes, however, no definite eccets were found. The mechanism of selective vulnerability of ischemia is not fully understood. An experiment of cerbellar ischemia was done in order to compare thr pathological change with that og thr hippocampus. %cerebella purkinje cells showed ishiemic cell damage following 10 min of comression ischemia. The alteration was, however, much faster than taht in the hippocampus. The underlying mechanism seems to be different. Focal cetebral ischiemia is more frequently sdeen in clinical case. To tsudy the reversibility of neurons in focal ischema, rats were subjected to permanent unilatearal middle cerebral artery occtusion. In ischemic region, rapid prograssion in infaction was noticed and slow process as is seen in the hippocampus was not recognized. On the other hand, in the distant areas of the brain, such as the thalamus, and substntia nigra, a slow buyt proufnd morphological changes were obsearved. Transizent focal cerebral ischemia in the rat is now being studeid in order to examine the possibility of reversible neuronal change following brief focal ischemia.
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