Axonal microtubules necessary for generation of sodium current in squid giant axons: I. pharmacological study on sodium current and restoration of sodium current by microtubule proteins and 260K protein

1983 ◽  
Vol 77 (2) ◽  
pp. 77-91 ◽  
Author(s):  
Gen Matsumoto ◽  
Michinori Ichikawa ◽  
Akira Tasaki ◽  
Hiromu Murofushi ◽  
Hikoichi Sakai
Keyword(s):  
Sodium Current ◽  
Pharmacological Study ◽  
Giant Axons

scholarly journals Quantitative Description of Sodium and Potassium Currents and Computed Action Potentials in Myxicola Giant Axons

1973 ◽  
Vol 61 (3) ◽  
pp. 361-384 ◽  
Author(s):  
L. Goldman ◽  
C. L. Schauf
Keyword(s):  
Action Potentials ◽  
Initial Conditions ◽  
Sodium Current ◽  
Quantitative Description ◽  
Potassium Conductance ◽  
Giant Axons ◽  
Sodium Conductance ◽  
Potassium Conductances ◽  
The Right ◽  
Sodium And Potassium

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.

scholarly journals Inactivation of the sodium current in squid giant axons by hydrocarbons

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

On the Persistent Sodium Current in Squid Giant Axons

2003 ◽  
Vol 89 (1) ◽  
pp. 640-644 ◽  
Author(s):  
John R. Clay
Keyword(s):  
Ion Channel ◽  
Sodium Current ◽  
Persistent Current ◽  
Sodium Ion ◽  
Ion Current ◽  
Peak Amplitude ◽  
Potential Range ◽  
Slow Inactivation ◽  
Giant Axons ◽  
Low Threshold

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.

scholarly journals Inactivation of the Sodium Current in Myxicola Giant Axons

1972 ◽  
Vol 59 (6) ◽  
pp. 659-675 ◽  
Author(s):  
L. Goldman ◽  
C. L. Schauf
Keyword(s):  
Steady State ◽  
Sodium Current ◽  
Voltage Characteristic ◽  
Current Voltage Characteristic ◽  
Inactivation Curve ◽  
Giant Axons ◽  
Sodium Conductance ◽  
Current Voltage ◽  
Steady State Inactivation ◽  
The Right

Experiments were conducted on Myxicola giant axons to determine if the sodium activation and inactivation processes are coupled or independent. The main experimental approach was to examine the effects of changing test pulses on steady-state inactivation curves. Arguments were presented to show that in the presence of a residual uncompensated series resistance the interpretation of the results depends critically on the manner of conducting the experiment. Analytical and numerical calculations were presented to show that as long as test pulses are confined to an approximately linear negative conductance region of the sodium current-voltage characteristic, unambiguous interpretations can be made. When examined in the manner of Hodgkin and Huxley, inactivation in Myxicola is quantitatively similar to that described by the h variable in squid axons. However, when test pulses were increased along the linear negative region of the sodium current-voltage characteristic, steady-state inactivation curves translate to the right along the voltage axis. The shift in the inactivation curve is a linear function of the ratio of the sodium, conductance of the test pulses, showing a 5.8 mv shift for a twofold increase in conductance. An independent line of evidence indicated that the early rate of development of inactivation is a function of the rise of the sodium conductance.

Effects of saxitoxin analogues and ligand competition on sodium currents of squid axons

1986 ◽  
Vol 251 (2) ◽  
pp. C159-C166 ◽  
Author(s):  
A. M. Frace ◽  
S. Hall ◽  
M. S. Brodwick ◽  
D. C. Eaton
Keyword(s):  
Binding Site ◽  
Voltage Clamp ◽  
Surface Potential ◽  
Sodium Current ◽  
Sodium Currents ◽  
Inward Current ◽  
Giant Axons ◽  
Sodium Conductance ◽  
Toxin Binding

Saxitoxin (STX) and several STX analogues from dinoflagellates (genus Protogonyaulax) block sodium conductance in squid giant axons with variable potencies. Toxins, analyzed under voltage clamp, are 21-sulfosaxitoxin, 21-sulfosaxitoxin 11 alpha-hydroxysulfate, 21-sulfosaxitoxin 11 beta-hydroxysulfate, (B1, C1, C2, respectively) and gonyautoxins 2 and 3. The potency sequence for the toxins examined is STX greater than gonyautoxin 3 greater than B1 greater than C2 greater than gonyautoxin 2 much greater than C1. Guanidine, when substituted for sodium in external seawater, reduced the potency of STX to block inward current but did not affect tetrodotoxin activity. Methylguanidine also reduced the ability of STX to block outward sodium current. Inhibitory constants for guanidine and methylguanidine were 116 and 187 mM, respectively. Competition can be explained by binding at or near the toxin binding site but not by surface potential alteration.

Synaptic potentials and threshold currents underlying spike production in motor giant axons of Aglantha digitale

1995 ◽  
Vol 74 (4) ◽  
pp. 1662-1670 ◽  
Author(s):  
R. W. Meech ◽  
G. O. Mackie
Keyword(s):  
Neuromuscular Junctions ◽  
Sodium Current ◽  
Giant Axon ◽  
Nerve Ring ◽  
Synaptic Delay ◽  
Similar Distribution ◽  
Axon Membrane ◽  
Postsynaptic Potentials ◽  
Giant Axons ◽  
Inward Currents

1. Motor giant axons that excite swimming muscles in the jelly-fish Aglantha digitale interface with units of the inner and outer nerve rings in the margin at the base of the bell. External recording electrodes were used to monitor electrical activity at different sites within the nerve ring while events in the motor giant axon were recorded with intracellular micropipettes placed within 100 microns of the synaptic area. In some experiments, 4- to 6-micron-diam patch pipettes were used to record in situ from ion channel clusters at different locations along the axon. 2. Independently propagating calcium and sodium spikes in the motor giant axon were found to arise from different excitatory postsynaptic potentials (EPSPs). Two separate inputs were identified; one EPSP class represented an input from the pacemaker system in the inner nerve ring, whereas another represented an input from the giant axon in the outer nerve ring. EPSPs from the two nerve rings had significantly different time courses and amplitudes. EPSPs from the ring giant axon reached a peak in little more than 1 ms, whereas EPSPs from the pacemaker system reached a maximum in approximately 7 ms. These slower EPSPs may be compound events composed of postsynaptic potentials from multiple synapses excited in series by the passage of the pacemaker neuron signal. 3. The threshold for the production of calcium spikes by the slow EPSPs of the pacemaker system (-51 +/- 2.2 mV, mean +/- SD; n = 5) corresponded well with the voltage at which a net inward “T”-type calcium current first appeared in recordings from axon membrane patches (-55 to -50 mV); the threshold for the initiation of the sodium spike by the fast EPSPs of the ring giant system (-32 +/- 1.2 mV, mean +/- SD; n = 6) corresponded well with the voltage at which a net inward sodium current first appeared (-35 to -30 mV). 4. Inward currents were rarely observed in membrane patches formed using pipettes with tips of < 1 micron OD. Even with 4-micron pipettes, patches of membrane were sometimes obtained with a channel population consisting exclusively of potassium channels; calcium and sodium currents were found in highly discrete areas (“hot spots”). Preliminary findings on the undersurface of the axon, which makes synaptic contact with the myoepithelium, are consistent with a similar distribution. 5. The pathway by which the ring giant excites the motor giant axon is not definitely known. The synaptic delay between the peak of the ring giant action potential (monitored externally) and the initial rise of the fast EPSP (1.64 +/- 0.15 ms, mean +/- SD; n = 21) would allow for transmission at two synapses, because single synaptic delays at neuromuscular junctions in Aglantha are approximately 0.7 ms at 12 degrees C. The mean synaptic delay at the slow EPSP synapse was 0.88 +/- 0.09 (SD) ms (n = 12). 6. The delay between the impulse in the ring giant axon and the subsequent excitation of the motor giant axon may permit the animal to withdraw its tentacles and so lower the drag that would otherwise reduce the effectiveness of any escape swim and might induce tentacle autotomy.

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