The equine periodic paralysis Na+ channel mutation alters molecular transitions between the open and inactivated states

The Journal of Physiology
W J HannaP H Backx

Abstract

1. The Na+ channel mutation associated with equine hyperkalaemic periodic paralysis (HPP) affects a highly conserved phenylalanine residue in an unexplored region of the alpha-subunit. This mutation was introduced into the rat skeletal muscle Na+ channel gene at the corresponding location (i.e. F1412L) for functional expression and characterization in Xenopus oocytes. 2. In comparison with wild-type (WT) channels, equine HPP channels showed clear evidence for disruption of inactivation: increased time-to-peak current, slowed rates of whole-cell current decay, significant increases in sustained current, rightward shifts in the steady-state inactivation curve by 9.5 mV, a 6-fold acceleration in the rate of recovery from inactivation at -80 mV, decreased number of blank single-channel sweeps, repetitive opening of single channels throughout depolarizing steps, increased open probability per sweep, and an increased mean open time. 3. The observed disruption of inactivation in HPP occurred without measurable changes in steady-state activation and first latency kinetics of channel opening. 4. Kinetic modelling demonstrates that the equine HPP phenotype can be simulated by altering the rate constants for transitions entering and leavi...Continue Reading

Citations

Mar 31, 2007·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Karin Jurkat-Rott, Frank Lehmann-Horn
Oct 3, 1999·Equine Veterinary Journal·T S MeyerH H Erickson
Aug 22, 2000·American Journal of Veterinary Research·M K AlbertsL M Homer
Oct 3, 1999·Physiological Reviews·F Lehmann-Horn, K Jurkat-Rott

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