Known mutations in CaV1.1 in hypokalemic periodic paralysis (HypoPP) occur at arginine residues of the voltage sensor domain and cause an anomalous inward gating pore current. By studying several HypoPP mutations, Wu et al. show that the magnitude of these gating pore currents is mutation specific.

Despite high similarity in sequence and structure, epithelial sodium channels display at least 50-fold higher sodium selectivity than acid-sensing ion channels. Here, Sheikh et al. show that sodium selectivity is likely achieved by different mechanisms in these related channels.

Beurg et al. report that the conductance of cochlear hair cell mechanotransducer channels inferred from single-channel events is larger than using noise analysis, which underestimates size due to filtering of fast openings. The difference leads to a first estimate of the channel activation time constant.

Kemp et al. show that the hERG channel activator RPR260243 restores the repolarizing current of a mutant variant of the channel associated with LQTS2 with little effect on its resurgent current. This drug represents a therapeutic opportunity for the treatment of arrhythmia associated with LQTS2.

Here, Björkgren et al. use whole-cell patch-clamp to show that the potassium channel Kir7.1 is stimulated by progesterone in the choroid plexus epithelium, as well as in other tissues in which Kir7.1 is present, and that the effect is specific to this steroid hormone.

Li et al. carry out molecular dynamics simulations of the K+ channels Shaker and KcsA to test whether a structural constriction of the non-conductive selectivity filter is a universal mechanism of C-type inactivation in K+ channels.

Vouga et al. show that the opioid receptor agonist loperamide is an inhibitor of large-conductance Ca2+-activated K+ (BK) channels that acts as a state-dependent pore blocker. Loperamide may exert its therapeutic effect partly by inhibiting potassium efflux in the intestine.