| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Research Abstract |
Inbred mutant El mice are highly suscrptible to convulsive seizures upon tossing stimulation. In this study, uptake and release of [^3H]aspartate(Asp), an excitatory amino acid, and [^3H]taurine, an inhibitory amino acid, into and from cerebral neurocortical slices using a perfusion system were investigated in both nonstimulated and stimulated El mice [El(-), El(+)] and in ddY mice, which do not have a convulsive disposition. Aspartate uptake and release in El(-) were lower than in ddY, and these in El(+) were significantly higher than in El(-). Taurine uptake in El(+) was lower than El(-), though no difference in uptake was found between ddY and El(-). Taurine release in El(-) was higher than ddY whereas the release in El(+) was lower than in El(-). These results suggest that acceleration of excitatory aspartate containing neurons and also suppression of inhibitory taurine containing neurons are involved in the seizure susceptibility in the El mice. [^3H]Asp release was decreased in ddY, when highe concentration (5mM) Asp was added in the superfusing solution, whereas it was increased in El(-) and no effect was observed in El(+). [^3H]Asp release was significantly increased in El(-), when high concentration of N-methyl-D-aspartate, an agonist of excitatory NMDA receptor, was added in the superfusing solution, whereas no effect was observed in ddY and El(+). These findings suggest that dysfunction of auto-receptor for Asp may relate to accelarated aspartate release in El(+), and that non-potassium depended release mechanism may concern to the increased release of Asp in El(-).
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