Role of TREK background potassium channels in nociception

Potassium channels with two pore domains (K2p) generate background K+ currents, which play a major role in membrane depolarization and cellular excitability. They are implicated in anesthesia, neuroprotection, depression, and pain. The K2p channel subfamily-TREK-1, TREK-2, and TRAAK-is modulated by pH, lipids (including polyunsaturated fatty acids), membrane stretching, and temperature. TREK-1 and TREK-2 are inactivated by phosphorylation of the G protein-coupled receptor (GPCR) via PKA and PKC. The analgesic effects of morphine are mediated by various signaling pathways downstream of ¿-opioid receptors, and TREK channels contribute to morphine-induced analgesia in mice. Here, we investigated the response of the dorsal root ganglion (DRG) in wild-type and triple-KO TREK-1-/- -TREK-2-/--TRAAK-/- mice to the application of morphine and capsaicin using calcium imaging. We also characterized an anti-TREK-2 antibody to study TREK-2 expression in DRG neurons.