On the persistent sodium current in squid giant axons.
R. F. Rakowski, D. C. Gadsby, and P. DeWeer have reported a persistent, tetrodotoxin-sensitive sodium ion current (I(NaP)) in squid giant axons having a low threshold (-90 mV) and a maximal inward amplitude of -4 microA/cm(2) at -50 mV. This report makes the case that most of I(NaP) is attributable to an ion channel mechanism distinct from the classical rapidly activating and inactivating sodium ion current, I(Na), which is also tetrodotoxin sensitive. The analysis of the contribution of I(Na) to I(NaP) is critically dependent on slow inactivation of I(Na). The results of this gating process reported here demonstrate that inactivation of I(Na) is complete in the steady-state for V > -40 mV, thereby making it unlikely that I(NaP) in this potential range is attributable to I(Na). Moreover, -90 mV is well below I(Na) threshold, as demonstrated by the C. A. Vandenberg and F. Bezanilla model of I(Na) gating in squid giant axons. Their model predicts a persistent current having a threshold of -60 mV and a peak amplitude of -25 microA/cm(2) at -20 mV. Modulation of this component by the slow inactivation process predicts a persistent current that is finite in the -60- to -40-mV range having a peak amplitude of -1 microA/cm(-2) at -50 mV. Subtraction of this current from the I(NaP) measurements yields the portion of I(NaP) that appears to be attributable to an ion channel mechanism distinct from I(Na).
Clay
John R
JR
Ion Channel Biophysics Unit, Basic Neurosciences Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA. jrclay@ninds.nih.gov
D000818:Animals; D001369:Axons / Q000502:physiology*; D049832:Decapodiformes; D008564:Membrane Potentials / Q000502:physiology; D008959:Models, Neurological; D018408:Patch-Clamp Techniques; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000502:physiology*
D015222:Sodium Channels; D012964:Sodium