NaV1.2 sodium channel loss paradoxically increases neuronal excitability and promotes seizures by preventing potassium channels from properly repolarizing neurons between action potentials.
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.
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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.
Spratt et al. (Sun,) reported a other. 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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