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Tandem JGP studies investigate how propofol affects voltage-gated sodium channels.


Jaffe underscores new research that identifies key roles for IP3 and TMEM16a in the fast block to polyspermy.

A new study reveals that conformational flexibility in the pore of a voltage-gated sodium channel may underlie slow inactivation.


The fast block to polyspermy is achieved in Xenopus laevis eggs by fertilization-induced depolarization. Wozniak et al. show that fertilization activates a signaling cascade involving phospholipase C, IP3, and intracellular Ca2+ release, which induces depolarization via Ca2+-activated Cl efflux.

In their preceding paper, Wozniak et al. show that fertilization increases intracellular Ca2+ in Xenopus laevis eggs by activating an IP3 signaling cascade. Here, they reveal that Ca2+ subsequently opens the Cl channel TMEM16A to allow Cl efflux, cell depolarization, and fast block to polyspermy.

HCN pacemaker channels are dually gated by hyperpolarizing voltages and cyclic nucleotide binding. Sunkara et al. show that each of the four binding sites promotes channel opening, most likely by exerting a turning momentum on the tetrameric intracellular gating ring.

Singlet oxygen modifies several different proteins within cells. Idikuda et al. show that, in the case of the sea urchin hyperpolarization-activated cyclic nucleotide–gated channel, a histidine residue in S6 is essential for the abolition of voltage-dependent inactivation by singlet oxygen.

The transient K+ current carried by Shaker channels is thought to play a role in low-frequency signal amplification in Drosophila melanogaster photoreceptors. By combining patch-clamp recordings with a physiological variability analysis, Frolov reveals its role in high-frequency signal transmission.

Despite extensive use in clinical practice, the mechanisms of propofol action on sodium channels are not fully understood. Yang et al. incorporate complementary biophysical approaches (electrophysiology and molecular dynamics simulations) to demonstrate that propofol inhibits two prokaryotic voltage-gated sodium channels, NaChBac and NavMs, by modulating both activation and inactivation gating.

General anesthetics inhibit voltage-gated sodium channels by unknown molecular mechanisms. Using computation-guided NMR and electrophysiology analyses, Wang et al. show that propofol binds to the prokaryotic sodium channel NaChBac at multiple distinct sites.

Voltage-gated sodium channels undergo slow inactivation during prolonged depolarization by means of a mechanism that is poorly understood. Chatterjee et al. study this process spectroscopically and reveal conformational flexibility of the pore region in the slow-inactivated state.

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