About the Cover
Cover design The figure shows spontaneous quantal ACh release (measured as miniature endplate potential frequency) at neuromuscular junctions of tottering mice, which are mutated in the P/Q-type Ca2+ channel ƒ1A subunit and have symptoms of ataxia and epilepsy. Spontaneous release is increased (~100%) compared with wild-type controls, and this effect is enhanced (to ~275%) upon slight depolarization by 10mM KCl (typical recordings are shown). ACh release in elevated KCl is greatly inhibited by 200nM ›agatoxin-IVA, a specific P-type channel blocker. The increase in spontaneous transmitter release may be explained by enlarged presynaptic influx of Ca2+ via mutant P/Q-type channels at resting membrane potential. From `Abnormal transmitter release at neuromuscular junctions of mice carrying the totttering ƒ1A Ca2+ channel mutation' by J. J. Plomp et al., 463471.
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