The molecular machinery of resurgent sodium current revealed.
Some TTX-sensitive sodium channels open transiently during recovery from inactivation, generating a "resurgent" sodium current that flows immediately following action potentials. In this issue of Neuron, Grieco and colleagues present evidence that resurgent sodium current results from a novel form of inactivation in which the cytoplasmic tail of the beta4 subunit acts as a classic open-channel blocker.
Bean
Bruce P
BP
Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
D000200:Action Potentials / Q000502:physiology; D001921:Brain / Q000502:physiology*; D002462:Cell Membrane / Q000502:physiology*; D015640:Ion Channel Gating / Q000502:physiology*; D062557:NAV1.6 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D021122:Protein Subunits / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology*; D062585:Voltage-Gated Sodium Channel beta-4 Subunit
D062557:NAV1.6 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins; D021122:Protein Subunits; C477263:SCN4B protein, human; C491046:Scn8a protein, mouse; D015222:Sodium Channels; D062585:Voltage-Gated Sodium Channel beta-4 Subunit