Kinetics of sodium current and gating current in the frog node of Ranvier

1986 ◽  
Vol 407 (1) ◽  
pp. 18-26 ◽  
Author(s):  
H. Meves ◽  
N. Rubly
Keyword(s):  
Sodium Current ◽  
Node Of Ranvier ◽  
Gating Current ◽  
Kinetics Of

scholarly journals Kinetics of intramembrane charge movement and sodium current in frog node of Ranvier.

1982 ◽  
Vol 79 (4) ◽  
pp. 571-602 ◽  
Author(s):  
J M Dubois ◽  
M F Schneider
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Sodium Current ◽  
Node Of Ranvier ◽  
Charge Movement ◽  
Intramembrane Charge Movement ◽  
Time Courses ◽  
Charge Movements ◽  
Kinetics Of ◽  
Microsecond Pulse

Intramembrane charge movement (Q) and sodium current (INa) were monitored in isolated voltage-clamped frog nodes of Ranvier, ON charge movements (QON) for pulses from the holding potential (-100 mV) to potentials V less than or equal to 0 mV followed single exponential time courses, whereas two exponentials were found for pulses to V greater than or equal to 20 mV. The voltage dependence of both QON and its time constant tauON indicated that the two ON components resolved at V greater than or equal to 20 mV were also present, though not resolvable, for pulses to V less than or equal to 0 mV. OFF charge movements (QOFF) monitored at various potentials were well described by single exponentials. When QOFF was monitored at -30 or -40 mV after a 200-microsecond pulse to +20 mV and QON was monitored at the same potential using pulses directly from -100 mV, tauON/tauOFF = 2.5 +/- 0.3. At a set OFF potential (-90 to -70 mV), tauOFF first increased with increasing duration tON of the preceding pulse to a given potential (0 to +30 mV) and then decreased with further increases in tON. The declining phase of tauOFF followed a time course similar to that of the decline in QOFF with tON. For the same pulse protocol, the OFF time constant tauNa for INA also first increased with tON but then remained constant over the tON interval during which tauOFF and QOFF were declining. After 200- or 300-microsecond pulses to +20, +20, or +50 mV, tauOFF/tauNa at -70 to -90 mV was 1.2 +/- 0.1. Similar tauOFF/tauNa ratios were predicted by channel models having three identical charged gating particles that can rapidly and reversibly form an immobile dimer or trimer after independently crossing the membrane from their OFF to their ON locations.

scholarly journals Charge Movement Associated with the Opening and Closing of the Activation Gates of the Na Channels

1974 ◽  
Vol 63 (5) ◽  
pp. 533-552 ◽  
Author(s):  
Clay M. Armstrong ◽  
Francisco Bezanilla
Keyword(s):  
Time Course ◽  
Sodium Current ◽  
Close Association ◽  
Outward Current ◽  
Transient Outward Current ◽  
Activation Process ◽  
Charge Movement ◽  
Gating Current ◽  
Dipolar Molecules ◽  
Opening And Closing

The sodium current (INa) that develops after step depolarization of a voltage clamped squid axon is preceded by a transient outward current that is closely associated with the opening of the activation gates of the Na pores. This "gating current" is best seen when permeant ions (Na and K) are replaced by relatively impermeant ones, and when the linear portion of capacitative current is eliminated by adding current from positive steps to that from exactly equal negative ones. During opening of the Na pores gating current is outward, and as the pores close there is an inward tail of current that decays with approximately the same time-course as INa recorded in Na-containing medium. Both outward and inward gating current are unaffected by tetrodotoxin (TTX). Gating current is capacitative in origin, the result of relatively slow reorientation of charged or dipolar molecules in a suddenly altered membrane field. Close association with the Na activation process is clear from the time-course of gating current, and from the fact that three procedures that reversibly block INa also block gating current: internal perfusion with Zn2+, prolonged depolarization of the membrane, and inactivation of INa with a short positive prepulse.

Slow components of the gating current in the frog node of Ranvier

1989 ◽  
Vol 8 (3) ◽  
pp. 432-434 ◽  
Author(s):  
H. Meves ◽  
J. -A. Pohl
Keyword(s):  
Node Of Ranvier ◽  
Gating Current

Kinetics of voltage-dependent sodium current in cultured frog Schwann cells

1991 ◽  
Vol 16 ◽  
pp. 1
Author(s):  
Takefumi Miyazaki ◽  
Junko Tasaka ◽  
Saeko Sakai ◽  
Toshio Hashiguchi ◽  
Tsuneo Tosaka
Keyword(s):  
Schwann Cells ◽  
Sodium Current ◽  
Voltage Dependent ◽  
Kinetics Of

Alterations of voltage-activated sodium current by a novel conotoxin from the venom of Conus gloriamaris

1995 ◽  
Vol 73 (3) ◽  
pp. 1295-1301 ◽  
Author(s):  
A. Hasson ◽  
K. J. Shon ◽  
B. M. Olivera ◽  
M. E. Spira
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Sodium Current ◽  
Land Snails ◽  
Calcium Currents ◽  
Inactivation Kinetics ◽  
The Novel ◽  
Inactivation Curve ◽  
Aplysia Neurons ◽  
Kinetics Of

1. The novel peptide toxin delta-conotoxin-GmVIA, recently purified by us from the mollusk-hunting snail Conus gloriamaris, induces convulsive-like contractions when injected into land snails but has no detectable effects in mammals. 2. At concentrations of 0.5-0.75 microM, the toxin induces action potential broadening and increased excitability of cultured Aplysia neurons. 3. Whole cell patch-clamp experiments on cultured Aplysia neurons revealed that the toxin does not alter potassium or calcium currents, but induces action potential broadening by slowing the inactivation kinetics of the sodium current. Under control conditions, the inactivation kinetics of the sodium current follows a single exponential with tau = 0.47 +/- 0.14 (SE) ms. After toxin application the sodium current inactivation is composed of two phases: an early phase with tau = 0.86 +/- 0.12 ms and a late phase of slowly inactivating sodium current with tau = 488 +/- 120 ms. In addition, the toxin shifts the voltage-dependent steady-state inactivation curve to more positive values and the steady-state activation curve to more negative values. These alterations are not associated with changes in the rise time or the peak value of the sodium current. 4. The novel delta-conotoxin-GmVIA, and the previously described "King Kong peptide," purified from another mollusk-hunting cone (Conus textile), share a similar cystein framework also found in the calcium channel blocking peptide omega-conotoxin but represent a new class of conotoxins with unusual specificity for molluscan sodium channels.

scholarly journals Slowing of sodium channel opening kinetics in squid axon by extracellular zinc.

1982 ◽  
Vol 79 (6) ◽  
pp. 935-964 ◽  
Author(s):  
W F Gilly ◽  
C M Armstrong
Keyword(s):  
Rate Constants ◽  
Membrane Surface ◽  
Outward Current ◽  
Forward Rate ◽  
Na Channel ◽  
Na Channels ◽  
Gating Current ◽  
Channel Opening ◽  
The Mean ◽  
Kinetics Of

The interaction of Zn ion on Na channels was studied in squid giant axons. At a concentration of 30 mM Zn2+ slows opening kinetics of Na channels with almost no alteration of closing kinetics. The effects of Zn2+ can be expressed as a "shift" of the gating parameters along the voltage axis, i.e., the amount of additional depolarization required to overcome the Zn2+ effect. In these terms the mean shifts caused by 30 mM Zn2+ were +29.5 mV for Na channel opening (on) kinetics (t1/2 on), +2 mV for closing (off) kinetics (tau off), and +8.4 mV for the gNa-V curve. Zn2+ does not change the shape of the instantaneous I-V curve for inward current, but reduces it in amplitude by a factor of or approximately 0.67. Outward current is unaffected. Effects of Zn2+ on gating current (measured in the absence of TTX) closely parallel its actions on gNa. On gating current kinetics are shifted by +27.5 mV, off kinetics by +6 mV, and the Q-V distribution by +6.5 mV. Kinetic modeling shows that Zn2+ slows the forward rate constants in activation without affecting backward rate constants. More than one of the several steps in activation must be affected. The results are not compatible with the usual simple theory of uniform fixed surface charge. They suggest instead that Zn2+ is attracted by a negatively charged element of the gating apparatus that is present at the outer membrane surface at rest, and migrates inward on activation.

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