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XB-ART-20285
Adv Exp Med Biol 1995 Jan 01;382:11-22.
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Molecular mechanisms of K+ channel blockade: 4-aminopyridine interaction with a cloned cardiac transient K+ (Kv1.4) channel.

Rasmusson RL , Zhang Y , Campbell DL , Comer MB , Castellino RC , Liu S , Morales MJ , Strauss HC .


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We studied the blocking effects of 4-aminopyridine (4-AP) on a Kv1.4 K+ channel. A permanently charged 4-AP derivative only produced block when applied intracellularly. 4-AP block accumulated from pulse to pulse indicating trapping of 4-AP in deactivated channels. For long trains of depolarizing pulses, 4-AP block increased with decreasing pulse duration. This increase took many pulses (> 10) to accumulate and was relieved by two to three subsequent pulses of 500 msec duration. We conclude that the time- and voltage-dependence of 4-AP block can not be accounted for solely by either simple pure open channel or pure closed channel blocking schemes. We propose that the data can be explained by a model in which 4-AP binding is most stable when the channel has a symmetric arrangement in the binding regions.

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Species referenced: Xenopus laevis
Genes referenced: kcna4