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• W2142095913 startingPage "1744" @default.
• W2142095913 abstract "Background: Small neurons of the dorsal root ganglion (DRG) express five of the nine known voltage-gated sodium channels. Each channel has unique biophysical characteristics which determine how it contributes to the generation of action potentials (AP). To better understand how AP amplitude is maintained in nociceptive DRG neurons and their centrally projecting axons, which are subjected to depolarization within the dorsal horn, we investigated the dependence of AP amplitude on membrane potential, and how that dependence is altered by the presence or absence of sodium channel Na v 1.8. Results: In small neurons cultured from wild type (WT) adult mouse DRG, AP amplitude decreases as the membrane potential is depolarized from −90 mV to −30 mV. The decrease in amplitude is best fit by two Boltzmann equations, having V 1/2 values of −73 and −37 mV. These values are similar to the V 1/2 values for steady-state fast inactivation of tetrodotoxin-sensitive (TTX-s) sodium channels, and the tetrodotoxin-resistant (TTX-r) Na v 1.8 sodium channel, respectively. Addition of TTX eliminates the more hyperpolarized V 1/2 component and leads to increasing AP amplitude for holding potentials of −90 to −60 mV. This increase is substantially reduced by the addition of potassium channel blockers. In neurons from Na v 1.8(-/-) mice, the voltage-dependent decrease in AP amplitude is characterized by a single Boltzmann equation with a V 1/2 value of −55 mV, suggesting a shift in the steady-state fast inactivation properties of TTX-s sodium channels. Transfection of Na v 1.8(-/-) DRG neurons with DNA encoding Na v 1.8 results in a membrane potential-dependent decrease in AP amplitude that recapitulates WT properties. Conclusion: We conclude that the presence of Na v 1.8 allows AP amplitude to be maintained in DRG neurons and their centrally projecting axons even when depolarized within the dorsal horn." @default.
• W2142095913 created "2016-06-24" @default.
• W2142095913 creator A5002957653 @default.
• W2142095913 creator A5060872309 @default.
• W2142095913 date "2007-01-01" @default.
• W2142095913 modified "2023-10-03" @default.
• W2142095913 title "Inactivation Properties of Sodium Channel Na_v1.8 Maintain Action Potential Amplitude in Small DRG Neurons in the Context of Depolarization" @default.
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• W2142095913 doi "https://doi.org/10.1186/1744-8069-3-12" @default.
• W2142095913 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1892009" @default.
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