| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Research Abstract |
In the first study, mitochondrial membrane potential was observed. Changes in mitochondrial membrane potential were measured in vivo at the site of a DC electrode using a potentiometric dye, JC-1. Two μl of dye (control group) or dye with oligomycin, an ATP synthetase inhibitor, (oligomycin group) was injected into the parieto-temporal cortex through the DC electrode. With the initiation of ischemia, a decrease in mitochondrial potential was observed within 20 seconds in the oligomycin group (earlier than the onset of DC deflection, p=0.02). In contrast, in the control group, mitochondrial potential was maintained at 91±5% of the pre-ischemia level for 118±38 seconds before showing full depolarization simultaneously with DC deflection. During the period of ischemia, the mitochondrial potential was higher in the control group (66±9%) than in the oligomycin group (46±8%, p=0.0002), whereas DC potential was lower in the control group (-18±3) than in the oligomycin group (-15±2mV, p=0.04). These observations suggest that mitochondria consume ATP during ischemia by reversing ATP synthetase activity, which compromises cellular membrane potential by consuming ATP. In the second study, therapeutic effects of cobalt were observed. The development of the ischemic core was analyzed using direct current (DC) potential and NADH fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. With intravenous injection of cobalt, the area of NADH fluorescence was decreased. Cobalt seems to ameliorate the mitochondrial energy balance in the penumbral region of focal ischemia.
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