Calcium gluconate has been empirically administered to hasten recovery of force during an episode of periodic paralysis. By using a genetically engineered mouse model, Uwera and colleagues show that low Ca2+ clearly promotes a loss of force in affected muscle, thereby providing the first evidence for the benefit of maintaining normal Ca2+ levels in this disorder.
In the current issue of JGP, Lamothe and Kurata explore the functional relationship between the Kv1.2 potassium channel, with Kvβ1.2 bound to the interior aspect of the channel, and Slc7a5, a component of the neutral amino acid transporter LAT1.
Ingestion of Ca2+ alleviates hyperkalemic periodic paralysis (HyperKPP) symptoms by an unknown mechanism. This study shows that lowering extracellular Ca2+ affects muscle contractility when the resting membrane potential is depolarized as in HyperKPP muscles and reduces the efficacy of salbutamol, a β2-adrenergic receptor agonist used to treat HyperKPP.
Polyamines regulate K+ efflux from cells by binding to K channels in a voltage-dependent manner. Suma et al. analyze how two polyamines, spermidine and spermine, bind and block the prokaryotic K channel MthK.
The neutral amino acid transporter Slc7a5 regulates the function and expression of the voltage-gated potassium channel Kv1.2. Lamothe and Kurata reveal that the effects of Slc7a5 are modified by the Kv1.2 accessory subunit Kvβ, while the properties of Kvβ-induced channel inactivation are modified by Slc7a5.
AMPA and NMDA receptors underlie several neuropathologies, but the detailed gating mechanism of these channels remains incompletely understood. Wilding and Huettner show that exposure to Cd opens AMPA and NMDA receptors with cysteine substitutions near the inner helix bundle-crossing gate.
A novel theoretical framework reveals more than one voltage-sensing pathway in the lateral membrane of outer hair cells
By comparing the measured displacement charge with a voltage-sensing model, Farrell et al. identify two hyperpolarized states and two reaction pathways in OHCs, suggesting that multiple pathways may allow these cells to amplify acoustic vibrations throughout the audible frequency range of mammals.