scholarly journals Analysis of sodium current fluctuations in the cut-open squid giant axon.

1984 ◽  
Vol 83 (2) ◽  
pp. 133-142 ◽  
Author(s):  
I Llano ◽  
F Bezanilla
Keyword(s):  
Sodium Channel ◽  
Sodium Channels ◽  
Sodium Current ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
Statistical Techniques ◽  
Current Fluctuations ◽  
Small Populations ◽  
Squid Axon ◽  
Single Sodium Channel

Patch pipettes were used to record the current arising from small populations of sodium channels in voltage-clamped cut-open squid axons. The current fluctuations associated with the time-variant sodium conductance were analyzed with nonstationary statistical techniques in order to obtain an estimate for the conductance of a single sodium channel. The results presented support the notion that the open sodium channel in the squid axon has only one value of conductance, 3.5 pS.

scholarly journals Interaction of n-alkylguanidines with the sodium channels of squid axon membrane.

1980 ◽  
Vol 76 (3) ◽  
pp. 315-335 ◽  
Author(s):  
G E Kirsch ◽  
J Z Yeh ◽  
J M Farley ◽  
T Narahashi
Keyword(s):  
Sodium Channel ◽  
Sodium Channels ◽  
Sodium Current ◽  
Time Dependent ◽  
Squid Axon ◽  
Axon Membrane ◽  
Inactivation Mechanism ◽  
Hydrophobic Binding ◽  
Sodium Inactivation ◽  
Guanidino Group

The effects of n-alkylguanidine derivatives on sodium channel conductance were measured in voltage clamped, internally perfused squid giant axons. After destruction of the sodium inactivation mechanism by internal pronase treatment, internal application of n-amylguanidine (0.5 mM) or n-octylguanidine (0.03 mM) caused a time-dependent block of sodium channels. No time-dependent block was observed with shorter chain derivatives. No change in the rising phase of sodium current was seen and the block of steady-state sodium current was independent of the membrane potential. In axons with intact sodium inactivation, an apparent facilitation of inactivation was observed after application of either n-amylguanidine or n-octylguanidine. These results can be explained by a model in which alkylguanidines enter and occlude open sodium channels from inside the membrane with voltage-independent rate constants. Alkylguanidine block bears a close resemblance to natural sodium inactivation. This might be explained by the fact that alkylguanidines are related to arginine, which has a guanidino group and is thought to be an essential amino acid in the molecular mechanism of sodium inactivation. A strong correlation between alkyl chain length and blocking potency was found, suggesting that a hydrophobic binding site exists near the inner mouth of the sodium channel.

scholarly journals Inhibitory effects of myrmicacin on the sodium channel in the squid giant axon.

1981 ◽  
Vol 57 (8) ◽  
pp. 314-317 ◽  
Author(s):  
Toshifumi TAKENAKA ◽  
Hidenori HORIE ◽  
Hideaki HORI ◽  
Tohru YOSHIOKA ◽  
Yozo IWANAMI
Keyword(s):  
Sodium Channel ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
Inhibitory Effects

Conduction velocity and gating current in the squid giant axon

1975 ◽  
Vol 189 (1094) ◽  
pp. 81-86 ◽  
Keyword(s):  
Sodium Channel ◽  
Conduction Velocity ◽  
Charged Particles ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
Gating Current ◽  
Giant Axons ◽  
Sodium Conductance ◽  
Conduction Velocities

As predicted by Hodgkin (1975), calculation of conduction velocities in squid giant axons shows that if each sodium channel is gated by charged particles moving in the membrane field there will be a maximum in the relation between sodium conductance and conduction velocity.

scholarly journals Effects of Intracellular Adenosine-5'-diphosphate and Orthophosphate on the Sensitivity of Sodium Efflux from Squid Axon to External Sodium and Potassium

1970 ◽  
Vol 56 (5) ◽  
pp. 583-620 ◽  
Author(s):  
Paul De Weer
Keyword(s):  
Creatine Phosphokinase ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
Squid Axon ◽  
Sodium Efflux ◽  
Excess Mg ◽  
Sodium And Potassium ◽  
External K

A study was made of sodium efflux from squid giant axon, and its sensitivity to external K and Na. When sodium efflux from untreated axons was strongly stimulated by Ko, Nao was inhibitory; when dependence on Ko was low, Nao had a stimulatory effect. Incipient CN poisoning or apyrase injection, which produces high intracellular levels of ADP1 and Pi, rendered sodium efflux less dependent on external K and more dependent on external Na. Injection of ADP, AMP, arginine, or creatine + creatine phosphokinase, all of which raise ADP levels without raising Pi levels, had the same effect as incipient CN poisoning. Pi injection had no effect on the K sensitivity of sodium efflux. Axons depleted of arginine and phosphoarginine by injection of arginase still lost their K sensitivity when the ATP:ADP ratio was lowered and regained it partially when the ratio was raised. Rough calculations show that sodium efflux is maximally Ko-dependent when the ATP:ADP ratio is about 10:1, becomes insensitive to Ko when the ratio is about 1:2, and is inhibited by Ko when the ratio is about 1:10. Deoxy-ATP mimicked ADP when injected into intact axons. Excess Mg, as well as Pi, inhibited both strophanthidin-sensitive and strophanthidin-insensitive sodium efflux. An outline is presented for a model which might explain the effects of ADP, Pi and deoxy-ATP.

scholarly journals RECTIFICATION AND INDUCTANCE IN THE SQUID GIANT AXON

1941 ◽  
Vol 25 (1) ◽  
pp. 29-51 ◽  
Author(s):  
Kenneth S. Cole
Keyword(s):  
Membrane Potential ◽  
Electrical Properties ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
Constant Current ◽  
Ion Permeability ◽  
Squid Axon ◽  
Axon Membrane ◽  
Piezoelectric Structure ◽  
In Series

Previous measurements have shown that the electrical properties of the squid axon membrane are approximately equivalent to those of a circuit containing a capacity shunted by an inductance and a rectifier in series. Selective ion permeability of a membrane separating two electrolytes may be expected to give rise to the rectification. A quasi-crystalline piezoelectric structure of the membrane is a plausible explanation of the inductance. Some approximate calculations of behavior of an axon with these membrane characteristics have been made. Fair agreement is obtained with the observed constant current subthreshold potential and impedance during the foot of the action potential. In a simple case a formal analogy is found between the calculated membrane potential and the excitability defined by the two factor formulations of excitation. Several excitation phenomena may then be explained semi-quantitatively by further assuming the excitability proportional to the membrane potential. Some previous measurements and subthreshold potential and excitability observations are not consistent with the circuit considered and indicate that this circuit is only approximately equivalent to the membrane.

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