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NaV1.2 sodium channel loss paradoxically increases neuronal excitability and promotes seizures by preventing potassium channels from properly repolarizing neurons between action potentials.
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NaV1.2 loss-of-function increases neuronal excitability by impairing potassium channel-mediated repolarization, providing a mechanistic explanation for how SCN2A loss can paradoxically promote seizures.
1.2 loss prevented potassium channels from properly repolarizing neurons between APs, increasing overall excitability by allowing neurons to reach threshold for subsequent APs more rapidly. This cell-intrinsic mechanism may, therefore, account for why SCN2A loss-of-function can paradoxically promote seizure.
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Spratt et al. (2021) studied this question. NaV1.2 sodium channel loss paradoxically increases neuronal excitability and promotes seizures by preventing potassium channels from properly repolarizing neurons between action potentials.
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