Dib-Hajj SD, Binshtok AM, Cummins TR, Jarvis MF, Samad T, Zimmermann K (2009)
Publication Type: Journal article, Review article
Publication year: 2009
Book Volume: 60
Pages Range: 65-83
Journal Issue: 1
DOI: 10.1016/j.brainresrev.2008.12.005
Pain is a major unmet medical need which has been causally linked to changes in sodium channel expression, modulation, or mutations that alter channel gating properties or current density in nociceptor neurons. Voltage-gated sodium channels activate (open) then rapidly inactivate in response to a depolarization of the plasma membrane of excitable cells allowing the transient flow of sodium ions thus generating an inward current which underlies the generation and conduction of action potentials (AP) in these cells. Activation and inactivation, as well as other gating properties, of sodium channel isoforms have different kinetics and voltage-dependent properties, so that the ensemble of channels that are present determine the electrogenic properties of specific neurons. Biophysical and pharmacological studies have identified the peripheral-specific sodium channels Na
APA:
Dib-Hajj, S.D., Binshtok, A.M., Cummins, T.R., Jarvis, M.F., Samad, T., & Zimmermann, K. (2009). Voltage-gated sodium channels in pain states: Role in pathophysiology and targets for treatment. Brain Research Reviews, 60(1), 65-83. https://doi.org/10.1016/j.brainresrev.2008.12.005
MLA:
Dib-Hajj, Sulayman D., et al. "Voltage-gated sodium channels in pain states: Role in pathophysiology and targets for treatment." Brain Research Reviews 60.1 (2009): 65-83.
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