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Hau-Jie Yau, Gytis Baranauskas and Marco Martina Flufenamic acid decreases neuronal excitability through modulation of voltage-gated sodium channel gating The Journal of Physiology 588

Article first published online: 14 OCT 2010 | DOI: 10.1113/jphysiol.2010.193037

Neuronal action potentials are generated by the interaction of two main voltage-gated conductances, one selectively permeable to sodium and the other to potassium ions. The gating properties of the ionic channels mediating these currents play a critical role in determining the threshold, frequency and shape of action potentials and therefore the modality of inter-neuronal communication. We studied the effects of flufenamic acid (FFA), a non-steroidal anti-inflammatory drug, on sodium channels. Our results show that FFA at near-clinical concentration has an inhibitory action on sodium currents. Biophysical analysis and computational simulations show that FFA acts by changing the voltage dependence of channels’ inactivation process. This effect heavily reduces the ability of neurons to discharge trains of action potentials, although the properties of individual action potentials are only slightly affected. The specific mode of action of FFA suggests that this molecule may be useful as anti-epileptic drug.

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