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• W1997955213 endingPage "8501" @default.
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• W1997955213 abstract "Neuronal excitability is critically determined by the properties of voltage-gated Na⁺ currents. Fast transient Na⁺ currents (<i>I</i>_NaT) mediate the fast upstroke of action potentials, whereas low-voltage-activated persistent Na⁺ currents (<i>I</i>_NaP) contribute to subthreshold excitation. Na⁺ channels are composed of a pore-forming α subunit and β subunits, which modify the biophysical properties of α subunits. We have examined the idea that the presence of β subunits also modifies the pharmacological properties of the Na⁺ channel complex using mice lacking either the β₁ (<i>Scn1b</i>) or β₂ (<i>Scn2b</i>) subunit. Classical effects of the anticonvulsant carbamazepine (CBZ), such as the use-dependent reduction of <i>I</i>_NaT and effects on <i>I</i>_NaT voltage dependence of inactivation, were unaltered in mice lacking β subunits. Surprisingly, CBZ induced a small but significant shift of the voltage dependence of activation of <i>I</i>_NaT and <i>I</i>_NaP to more hyperpolarized potentials. This novel CBZ effect on <i>I</i>_NaP was strongly enhanced in <i>Scn1b</i> null mice, leading to a pronounced increase of <i>I</i>_NaP within the subthreshold potential range, in particular at low CBZ concentrations of 10–30 μm. A combination of current-clamp and computational modeling studies revealed that this effect causes a complete loss of CBZ efficacy in reducing repetitive firing. Thus, β subunits modify not only the biophysical but also the pharmacological properties of Na⁺ channels, in particular with respect to <i>I</i>_NaP. Consequently, altered expression of β subunits in other neurological disorders may cause altered neuronal sensitivity to drugs targeting Na⁺ channels." @default.
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• W1997955213 date "2010-06-23" @default.
• W1997955213 modified "2023-10-15" @default.
• W1997955213 title "Efficacy Loss of the Anticonvulsant Carbamazepine in Mice Lacking Sodium Channel Subunits via Paradoxical Effects on Persistent Sodium Currents" @default.
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• W1997955213 doi "https://doi.org/10.1523/jneurosci.1534-10.2010" @default.
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