| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
It has been reported that glucose suppresses sodium channal and hyperpolarizes resting membrane potential with its leakage conductance increased (Hironaka et al., 1981, 8th INTN. Pharmacol.). Although each effect is not so marked, they all together may act as to inhibit the excitation of nerve cells. Especially glucose exists in blood with a high and variable concentrations, rapidly reflecting to a demand in the brain. Therefore, it is very likely that glucose plays a regulatory role in the brain in terms of the excitability of the nerve cells.
In the present study, we intended to elucidate ionic mechanism of the leakege conductance increase induced by glucose using a voltage clamp method with artificial partitions. Special efforts were made to reduce the short-circuiting current so that a minute amount of leakage current across the axon membrane could be measured. First, the length of the insulating gap was taken rether long than ever done and a liquid paraffin pool was introduced in the middle of the vaseline seal. Second, the fluid surrounding the axon was thoroughly removed by mixing adsorbents with the paraffin. Further, to mrasure the absolute value of the resting membrane potential with external electrodes, the exon membrane in one side of the external pools was cut open and filled with an internal solution, constituting a potential-measuring system. The results obtained were the same as expected from the previous studies. Namely, glucose increases the lakage conductance by mainly elevating potassium permeability.
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