Sodium channels: grit, determination, and persistence.
Persistent sodium channel activity modulates neuronal gain in a neurotransmitter-dependent fashion. Previous studies have suggested that persistent and spike-related sodium channel activities are mediated by separate species. In this issue of Neuron, Taddese and Bean (2002) show that a single channel population is sufficient to explain both gating behaviors. A simple allosteric model is provided that can explain the results.
Huguenard
John R
JR
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism*; D002490:Central Nervous System / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
D015222:Sodium Channels