Analysis of iconic and gating currents of wild type and mutated BK channels reveals a strong inhibition of this channel by extracellular acidification and elucidates the underlying mechanism that is potentially applicable to other voltage-dependent cation channels.
C-terminus mediated inhibition is one emerging modality of intervention for L-type Ca2+ channels, which coordinate multiple motifs to acutely tune Ca2+ current and Ca2+ influx down to the lower limits preset by end-stage Ca2+-dependent inactivation.
The mammalian potassium channel KCa3.1, which is important for T- and B-cell activation, is inhibited by cytoplasmic copper, mediated by a histidine residue (His358) that is phosphorylated to activate the channel.
Computational modeling and analysis of mouse neural population data finds that the excitation/inhibition imbalance theory of brain disorders is too limited to account for key changes in neural activity statistics.
A cationic molecule derived from an uncharged Cav2.2 calcium channel inhibitor powerfully inhibits both sodium and calcium channels with extracellular application and inhibits both pain and neurogenic inflammation.
Pro-nociceptive and pro-inflammatory TRPM3 (transient receptor potential melastatin 3) channels, expressed in somatosensory neurons, are inhibited by activation of Gαi-coupled receptors, such as µ-opioid receptors, in vitro and in vivo.