Abstract
The voltage dependent sodium current determines the upstroke of the action potential, and it is therefore one of the determinant factors for neuronal excitability. The steep voltage dependence of activation as well as inactivation in combination with its fast kinetics imply that even relatively small changes in sodium current properties will have a significant influence on, for example, cell firing frequency. It is therefore not surprising that the majority of antiepileptic drugs (AEDs) exert their action by modulating sodium current properties that are relevant for cell firing.1 The aim of this study is to parameterize the sodium current in CA1 hippocampal pyramidal cells using the classical description originally provided by Hodgkin and Huxley2, 3 employing voltage clamp data obtained from neurons acutely isolated from the rat hippocampus. Such a description does not comprise every possible detail of the present knowledge of the sodium channel. Nevertheless it appears to be sufficient to describe the changes observed in the inactivation function of the sodium current in neurons isolated from the epileptic focus in rats that were either kindled4 or in which a status epilepticus model was generated.5
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Wadman, W.J., Min, R., Sun, G. (2005). Sodium Current Properties in Different Models of Epilepsy. In: Corcoran, M.E., Moshé, S.L. (eds) Kindling 6. Advances in Behavioral Biology, vol 55. Springer, Boston, MA. https://doi.org/10.1007/0-387-26144-3_7
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DOI: https://doi.org/10.1007/0-387-26144-3_7
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