Axonal microtubules necessary for generation of sodium current in squid giant axons: II. Effect of colchicine upon asymmetrical displacement current

1983 ◽  
Vol 77 (2) ◽  
pp. 93-99 ◽  
Author(s):  
Gen Matsumoto ◽  
Michinori Ichikawa ◽  
Akira Tasaki
1973 ◽  
Vol 61 (3) ◽  
pp. 361-384 ◽  
Author(s):  
L. Goldman ◽  
C. L. Schauf

All analysis of the sodium and potassium conductances of Myxicola giant axons was made in terms of the Hodgkin-Huxley m, n, and h variables. The potassium conductance is proportional to n2. In the presence of conditioning hyperpolarization, the delayed current translates to the right along the time axis. When this effect was about saturated, the potassium conductance was proportional to n3. The sodium conductance was described by assuming it proportional to m3h. There is a range of potentials for which τh and h∞ values fitted to the decay of the sodium conductance may be compared to those determined from the effects of conditioning pulses. τh values determined by the two methods do not agree. A comparison of h∞ values determined by the two methods indicated that the inactivation of the sodium current is not governed by the Hodgkin-Huxley h variable. Computer simulations show that action potentials, threshold, and subthreshold behavior could be accounted for without reference to data on the effects of initial conditions. However, recovery phenomena (refractoriness, repetitive discharges) could be accounted for only by reference to such data. It was concluded that the sodium conductance is not governed by the product of two independent first order variables.


1985 ◽  
Vol 48 (4) ◽  
pp. 617-622 ◽  
Author(s):  
J.R. Elliott ◽  
D.A. Haydon ◽  
B.M. Hendry ◽  
D. Needham
Keyword(s):  

1976 ◽  
Vol 193 (1113) ◽  
pp. 469-475 ◽  

Asymmetrical displacement currents similar to those identified elsewhere as sodium gating currents have been recorded in the giant axon of Myxicola , and their characteristics are briefly described.


2003 ◽  
Vol 89 (1) ◽  
pp. 640-644 ◽  
Author(s):  
John R. Clay

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 INaP that appears to be attributable to an ion channel mechanism distinct from I Na.


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