scholarly journals ANESTHETIC AND CALCIUM ACTION IN THE VOLTAGE CLAMPED SQUID GIANT AXON

1959 ◽  
Vol 42 (4) ◽  
pp. 793-802 ◽  
Author(s):  
A. M. Shanes ◽  
W. H. Freygang ◽  
H. Grundfest ◽  
E. Amatniek

Changes in spike configuration and in the inward and outward currents of voltage-clamped axons agree in indicating that the increases in permeability to sodium and potassium ions during activity are depressed by procaine and cocaine and augmented by calcium. At low levels of depolarization, the effect of the multivalent ion is similar to that of the local anesthetics, in keeping with their similar effects on the threshold of excitability. The reduction of membrane conductance at rest requires a higher concentration of the drugs than that needed to affect the increase in permeability with activity.

1953 ◽  
Vol 37 (1) ◽  
pp. 25-37 ◽  
Author(s):  
Harry Grundfest ◽  
Abraham M. Shanes ◽  
Walter Freygang

Decrease of the sodium concentration of the medium depresses both the spike and the associated impedance change in almost identical fashion. Elevation of the potassium level also depresses both phenomena, but affects the impedance change more than the spike; it slows the return to the initial impedance level. The effects on the threshold to brief square waves are also described. These results appear largely accounted for by the observations of Hodgkin and Huxley with the voltage clamp technique and by their recent hypothesis as to nature of the spike processes.


2015 ◽  
Vol 26 (10) ◽  
pp. 1550112 ◽  
Author(s):  
James Christopher S. Pang ◽  
Johnrob Y. Bantang

We utilize the original Hodgkin–Huxley (HH) model to consider the effects of defective ion channels to the temporal response of neurons. Statistics of firing rate and inter-spike interval (ISI) reveal that production of action potentials (APs) in neurons is not sensitive to changes in membrane conductance for sodium and potassium ions, as well as to the reversal potential for sodium ions, as long as the relevant parameters do not exceed 13% from their normal levels. We also found that blockage of a critical fraction of either sodium or potassium channels (dependent on constant input current) respectively limits the firing activity or increases spontaneous spiking activity of neurons. Our model may be used to guide experiment designs related to ion channel control drug development.


1967 ◽  
Vol 50 (3) ◽  
pp. 533-549 ◽  
Author(s):  
R. A. Sjodin ◽  
L. J. Mullins

The efflux of labeled and unlabeled potassium ions from the squid giant axon has been measured under a variety of experimental conditions. Axons soaked in sea water containing 42K ions lost radioactivity when placed in inactive sea water according to kinetics which indicate the presence of at least two cellular compartments. A rapidly equilibrating superficial compartment, probably the Schwann cell, was observed to elevate the specific activity of 42K lost from such axons to K-free sea water for a period of hours. The extra radioactive potassium loss from such axons during stimulation, however, was shown to have a specific activity identical within error to that measured in the axoplasm at the end of the experiment. The same was shown for the extra potassium loss occurring during passage of a steady depolarizing current. Axons placed in sea water with an elevated potassium ion concentration (50 mM) showed an increased potassium efflux that was in general agreement with the accompanying increase in membrane conductance. The efflux of potassium ions observed in 50 mM K sea water at different membrane potentials did not support the theory that the potassium fluxes obey the independence principle.


1970 ◽  
Vol 56 (5) ◽  
pp. 583-620 ◽  
Author(s):  
Paul De Weer

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.


1957 ◽  
Vol 40 (6) ◽  
pp. 859-885 ◽  
Author(s):  
Ichiji Tasaki ◽  
Susumu Hagiwara

1. Intracellular injection of tetraethylammonium chloride (TEA) into a giant axon of the squid prolongs the duration of the action potential without changing the resting potential (Fig. 3). The prolongation is sometimes 100-fold or more. 2. The action potential of a giant axon treated with TEA has an initial peak followed by a plateau (Fig. 3). The membrane resistance during the plateau is practically normal (Fig. 4). Near the end of the action potential, there is an apparent increase in the membrane resistance (Fig. 5D and Fig. 6, right). 3. The phenomenon of abolition of action potentials was demonstrated in the squid giant axon treated with TEA (Fig. 7). Following an action potential abolished in its early phase, there is no refractoriness (Fig. 8). 4. By the method of voltage clamp, the voltage-current relation was investigated on normal squid axons as well as on axons treated with TEA (Figs. 9 and 10). 5. The presence of stable states of the membrane was demonstrated by clamping the membrane potential with two voltage steps (Fig. 11). Experimental evidence was presented showing that, in an "unstable" state, the membrane conductance is not uniquely determined by the membrane potential. 6. The effect of low sodium water was investigated in the axon treated with TEA (Fig. 12). 7. The similarity between the action potential of a squid axon under TEA and that of the vertebrate cardiac muscle was stressed. The experimental results were interpreted as supporting the view that there are two stable states in the membrane. Initiation and abolition of an action potential were explained as transitions between the two states.


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