Neurophysiological and molecular approach for evaluating mechanism of pathogenesis of febrile seizure

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Recently gene abnormality which codes alpha or beta subunit of the sodium channel such as SCN1A was revealed in a case with febrile seizures. The purpose of this study is to evaluate the effect of increased temperature to the sodium channel by method of patch clamp. In our previous research, we disclosed that the incidence of seizures was significantly increased in cases of children with fever when they were given antihistaminic agents. We evaluated the effect of first-generation antihistaminic agents to 2 potassium channels. The antihistaminics suppressed potassium channels, especially to M-current. We suggested that the standard antihistaminic agent, pyrilamine acted directly on the M-channel pores. H2-receptor antagonists did not affect the M-channel. The inhibition of M channels may be involved in the neurotoxic effects of first-generation antihistaminics overdose.In ordinary patch clamp experiments, the temperature of fluid in the chamber is kept about 25℃, but we tried to make the environmental temperature higher. However, the ordinary Y-tube did not make steady temperature. Then we created loop shaped Y-tube which successfully kept the temperature of the medium about 35℃. Eventually we could record sodium channel current at 40℃.