Slow inactivation in voltage-gated sodium channels: molecular substrates and contributions to channelopathies.
Slow inactivation in voltage-gated sodium channels is a biophysical process that governs the availability of sodium channels over extended periods of time. Slow inactivation, therefore, plays an important role in controlling membrane excitability, firing properties, and spike frequency adaptation. Defective slow inactivation is associated with several diseases of cell excitability, such as hyperkalemic periodic paralysis, myotonia, idiopathic ventricular fibrillation and long-QT syndrome. These associations underscore the physiological importance of this phenomenon. Nevertheless, our understanding of the molecular substrates for slow inactivation is still fragmentary. This review covers the current state of knowledge concerning the molecular underpinnings of slow inactivation, and its relationship with other biophysical processes of voltage-gated sodium channels.
Vilin
Y Y
YY
Department of Biology, Utah State University, Logan 84322, USA.
Ruben
P C
PC
D000818:Animals; D004594:Electrophysiology; D006801:Humans; D007700:Kinetics; D008133:Long QT Syndrome / Q000378:metabolism; D009154:Mutation; D009222:Myotonia / Q000378:metabolism; D010243:Paralysis / Q000378:metabolism; D011485:Protein Binding; D011487:Protein Conformation; D015222:Sodium Channels / Q000235:genetics* / Q000378:metabolism*; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000378:metabolism
D015222:Sodium Channels