Highly temperature-sensitive behavior of voltage-gated potassium channels provides a mechanistic model for how heat-activated TRP channels serve as temperature and pain sensors.
ZDHHC14 controls palmitoylation and axon initial segment targeting of PSD93 and Kv1-family potassium channels, events that are essential for normal neuronal excitability.
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.
Loss of potassium channel activity from fast-spiking interneurons increases their excitability leading to unexpectedly increased fast excitatory transmission and seizure susceptibility.
An integrative structural biology approach provides refined models of the KCNQ1-KCNE1 channel complex, which propose a new mechanism to explain how KCNE1 modulates KCNQ1 channel activation.
Serotonin neurons in chronically isolated mice become less responsive to excitatory stimulation, but inhibiting a distinctive calcium-activated potassium channel can restore both neuronal activity and behavior.