Sodium channel inactivation defects are associated with acetazolamide-exacerbated hypokalemic periodic paralysis

2001 ◽  
Vol 50 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Sa�d Bendahhou ◽  
Theodore R. Cummins ◽  
Robert C. Griggs ◽  
Ying-Hui Fu ◽  
Louis J. Pt�?ek
Keyword(s):  
Sodium Channel ◽  
Periodic Paralysis ◽  
Hypokalemic Periodic Paralysis ◽  
Channel Inactivation ◽  
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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