Potassium channels control neuronal excitability through influence over the duration, frequency and amplitude of action potentials. Potassium channels that are active at rest inhibit depolarization toward firing threshold, and thus suppress excitation. Conversely, potassium channels activated at depolarized potentials do not interfere with rise to threshold, but do facilitate recovery and repetitive firing. Tandem pore domain K+ channels (K2p) produce leak K+ current which stabilizes negative membrane potential and counter balances depolarization. These channels are regulated by voltage independent mechanisms such as membrane stretch, pH, temperature (Goldstein et al. 2005, Lotshaw 2007, Enyedi & Czirja 2010). Tandem pore domain K+ channels have been classified into six subfamilies; tandem pore domains in weak rectifying K+ channel (TWIK), TWIK-related K+ channel (TREK), TWIK-related acid-sensitive K+ channel (TASK), TWIK-related alkaline pH-activated K+ channel (TALK), tandem pore domain halothane-inhibted K+ channel (THIK), TWIK-releated spinal cord K+ channel). outwardly rectifying channel that is sensitive to changes in extracellular pH and is inhibited by extracellular acidification. Also referred to as an acid-sensitive potassium channel, it is activated by the anesthetics halothane and isoflurane.
potassium channel activity of KCNK dimers [plasma membrane]