Intracellular binding of cationized ferritin prolongs the time course of sodium channel inactivation in squid giant axons

1986 ◽  
Vol 89 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Kishio Furuya ◽  
Hiroshi Hirano ◽  
Fumiaki Nishiyama ◽  
Fumio Kukita ◽  
Shunichi Yamagishi
Keyword(s):  
Sodium Channel ◽  
Time Course ◽  
Cationized Ferritin ◽  
Giant Axons ◽  
Channel Inactivation ◽  
Sodium Channel Inactivation ◽  
Intracellular Binding

scholarly journals Removal of sodium channel inactivation in squid axon by the oxidant chloramine-T.

1985 ◽  
Vol 86 (2) ◽  
pp. 289-302 ◽  
Author(s):  
G K Wang ◽  
M S Brodwick ◽  
D C Eaton
Keyword(s):  
Sodium Channel ◽  
Time Course ◽  
Removal Rate ◽  
Potassium Currents ◽  
Activation Process ◽  
Sodium Currents ◽  
Methionine Residue ◽  
Channel Inactivation ◽  
Sodium Channel Inactivation ◽  
Chloramine T

We have investigated the effects of a mild oxidant, chloramine-T(CT), on the sodium and potassium currents of squid axons under voltage-clamp conditions. Sodium channel inactivation of squid giant axons can be completely removed by CT at neutral pH. Internal and external CT treatment are both effective. CT apparently removes inactivation in an irreversible, all-or-none manner. The activation process of sodium channels is little affected, as judged from the voltage dependence of peak sodium currents, the rising phase of sodium currents, and the time course of tail currents following the repolarization. The removal of inactivation by CT is pH-dependent; higher pH decreases the removal rate, whereas lower pH increases it. Internal metabisulfite, a strong reductant, does not protect inactivation from the action of external CT, nor does external metabisulfite protect from internal CT application. CT slightly depresses the peak potassium currents at comparable concentrations but has no apparent effects on their kinetics. Our results suggest that the neutral form of CT modifies an embedded methionine residue that is involved in sodium channel inactivation.

Solution Structure of the Sodium Channel Inactivation Gate†,‡

Biochemistry ◽  
1999 ◽  
Vol 38 (3) ◽  
pp. 855-861 ◽  
Author(s):  
Carol A. Rohl ◽  
Faye A. Boeckman ◽  
Carl Baker ◽  
Todd Scheuer ◽  
William A. Catterall ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Solution Structure ◽  
Channel Inactivation ◽  
Sodium Channel Inactivation

Modification of Synaptic Transmission and Sodium Channel Inactivation by the Insect-Selective Scorpion Toxin LqhαIT

2000 ◽  
Vol 83 (3) ◽  
pp. 1181-1187 ◽  
Author(s):  
Daewoo Lee ◽  
Michael Gurevitz ◽  
Michael E. Adams
Keyword(s):  
Steady State ◽  
Sodium Channel ◽  
Transmitter Release ◽  
House Fly ◽  
The Body ◽  
Scorpion Toxin ◽  
Nerve Endings ◽  
Channel Inactivation ◽  
Sodium Channel Inactivation ◽  
Steady State Inactivation

The peptide LqhαIT is an α-scorpion toxin that shows significant selectivity for insect sodium channels over mammalian channels. We examined the symptoms of LqhαIT-induced paralysis and its neurophysiological correlates in the house fly ( Musca domestica). Injection of LqhαIT into fly larvae produced hyperactivity characterized by continuous, irregular muscle twitching throughout the body. These symptoms were correlated with elevated excitability in motor units caused by two physiological effects of the toxin: 1) increased transmitter release and 2) repetitive action potentials in motor nerves. Increased transmitter release was evident as augmentation of neurally evoked synaptic current, and this was correlated with an increased duration of action potential–associated current (APAC) in loose patch recordings from nerve terminals. Repetitive APACs were observed to invade nerve endings. The toxin produced marked inhibition of sodium current inactivation in fly central neurons, which can account for increased duration of the APAC and elevated neurotransmitter release at the neuromuscular junction. Steady-state inactivation was shifted significantly to more positive potentials, whereas voltage-dependent activation of the channels was not affected. The shift in steady-state inactivation provides a mechanism for inducing repetitive activity in motoneurons. The effects of LqhαIT on sodium channel inactivation in motor nerve endings can account both for increased transmitter release and repetitive activity leading to hyperactivity in affected insects.

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