The effect ofTityus serrulatus scorpion toxin γ on Na channels in neuroblastoma cells

1984 ◽  
Vol 401 (3) ◽  
pp. 297-303 ◽  
Author(s):  
Henk P. M. Vijberberg ◽  
David Pauron ◽  
Michel Lazdunski
Keyword(s):  
Neuroblastoma Cells ◽  
Scorpion Toxin ◽  
Na Channels

A proteomic analysis of the early secondary molecular effects caused by Cn2 scorpion toxin on neuroblastoma cells

2014 ◽  
Vol 111 ◽  
pp. 212-223 ◽  
Author(s):  
Martha Pedraza Escalona ◽  
Cesar V.F. Batista ◽  
Rita Restano Cassulini ◽  
Marisol Sandoval Rios ◽  
Fredy I. Coronas ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Neuroblastoma Cells ◽  
Scorpion Toxin ◽  
Molecular Effects

Conversion of a scorpion toxin agonist into an antagonist highlights an acidic residue involved in voltage sensor trapping during activation of neuronal Na + channels

2004 ◽  
Vol 18 (6) ◽  
pp. 683-689 ◽  
Author(s):  
Karbat Izhar ◽  
Cohen Lior ◽  
Gilles Nicolas ◽  
Gordon Dalia ◽  
Gurevitz Michael
Keyword(s):  
Voltage Sensor ◽  
Scorpion Toxin ◽  
Na Channels

scholarly journals Gating of Na channels. Inactivation modifiers discriminate among models.

1987 ◽  
Vol 89 (2) ◽  
pp. 253-274 ◽  
Author(s):  
T Gonoi ◽  
B Hille
Keyword(s):  
Proteolytic Enzymes ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Cell Voltage ◽  
Na Channel ◽  
Na Channels ◽  
Negative Direction ◽  
Conductance Curve ◽  
Voltage Curve ◽  
Na Currents

Macroscopic Na currents were recorded from N18 neuroblastoma cells by the whole-cell voltage-clamp technique. Inactivation of the Na currents was removed by intracellular application of proteolytic enzymes, trypsin, alpha-chymotrypsin, papain, or ficin, or bath application of N-bromoacetamide. Unlike what has been reported in squid giant axons and frog skeletal muscle fibers, these treatments often increased Na currents at all test pulse potentials. In addition, removal of inactivation gating shifted the midpoint of the peak Na conductance-voltage curve in the negative direction by 26 mV on average and greatly prolonged the rising phase of Na currents for small depolarizations. Polypeptide toxins from Leiurus quinquestriatus scorpion and Goniopora coral, which slow inactivation in adult nerve and muscle cells, also increase the peak Na conductance and shift the peak conductance curve in the negative direction by 7-10 mV in neuroblastoma cells. Control experiments argue against ascribing the shifts to series resistance artifacts or to spontaneous changes of the voltage dependence of Na channel kinetics. The negative shift of the peak conductance curve, the increase of peak Na currents, and the prolongation of the rise at small depolarization after removal of inactivation are consistent with gating kinetic models for neuroblastoma cell Na channels, where inactivation follows nearly irreversible activation with a relatively high, voltage-independent rate constant and Na channels open only once in a depolarization. As the same kind of experiment does not give apparent shifting of activation and prolongation of the rising phase of Na currents in adult axon and muscle membranes, the Na channels of these other membranes probably open more than once in a depolarization.

Tetrodotoxin-resistant Na+channels in human neuroblastoma cells are encoded by new variants of Nav1.5/SCN5A

2005 ◽  
Vol 22 (4) ◽  
pp. 793-801 ◽  
Author(s):  
Shao-Wu Ou ◽  
Asako Kameyama ◽  
Li-Ying Hao ◽  
Masahisa Horiuchi ◽  
Etsuko Minobe ◽  
...  
Keyword(s):  
Neuroblastoma Cells ◽  
Na Channels ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

One-to-one binding of a purified scorpion toxin to Na channels

Nature ◽  
1977 ◽  
Vol 266 (5601) ◽  
pp. 465-468 ◽  
Author(s):  
HARUMASA OKAMOTO ◽  
KUNITARO TAKAHASHI ◽  
NAOHIDE YAMASHITA
Keyword(s):  
Scorpion Toxin ◽  
Na Channels ◽  
One To One

scholarly journals Veratridine modifies open sodium channels.

1988 ◽  
Vol 91 (3) ◽  
pp. 421-443 ◽  
Author(s):  
S Barnes ◽  
B Hille
Keyword(s):  
Single Channel ◽  
Neuroblastoma Cells ◽  
Cell Voltage ◽  
State Dependence ◽  
Na Channel ◽  
Na Channels ◽  
Pipette Solution ◽  
Whole Cell ◽  
Current Activation ◽  
Normal Current

The state dependence of Na channel modification by the alkaloid neurotoxin veratridine was investigated with single-channel and whole-cell voltage-clamp recording in neuroblastoma cells. Several tests of whole-cell Na current behavior in the presence of veratridine supported the hypothesis that Na channels must be open in order to undergo modification by the neurotoxin. Modification was use dependent and required depolarizing pulses, the voltage dependence of production of modified channels was similar to that of normal current activation, and prepulses that caused inactivation of normal current had a parallel effect on the generation of modified current. This hypothesis was then examined directly at the single-channel level. Modified channel openings were easily distinguished from normal openings by their smaller current amplitude and longer burst times. The modification event was often seen as a sudden, dramatic reduction of current through an open Na channel and produced a somewhat flickery channel event having a mean lifetime of 1.6 s at an estimated absolute membrane potential of -45 mV (23 degrees C). The modified channel had a slope conductance of 4 pS, which was 20-25% the size of the slope conductance of normal channels with the 300 mM NaCl pipette solution used. Most modified channel openings were initiated by depolarizing pulses, began within the first 10 ms of the depolarizing step, and were closely associated with the prior opening of single normal Na channels, which supports the hypothesis that modification occurs from the normal open state.

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