J Neurophysiol (January 1, 2003). 10.1152/jn.00652.2002
Submitted on Submitted 9 August 2002; accepted in final form. 17 September 2002

REPORT

On the Persistent Sodium Current in Squid Giant Axons

Ion Channel Biophysics Unit, Basic Neurosciences Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892; and the Marine Biological Laboratory, Woods Hole, Massachusetts 02543

Clay, John R. On the Persistent Sodium Current in Squid Giant Axons. J. Neurophysiol. 89: 640-644, 2003. 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 µA/cm² 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 µA/cm² 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 1µA/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.