TY - JOUR T1 - Slack Channels Expressed in Sensory Neurons Control Neuropathic Pain in Mice JF - The Journal of Neuroscience JO - J. Neurosci. SP - 1125 LP - 1135 DO - 10.1523/JNEUROSCI.2423-14.2015 VL - 35 IS - 3 AU - Ruirui Lu AU - Anne E. Bausch AU - Wiebke Kallenborn-Gerhardt AU - Carsten Stoetzer AU - Natasja Debruin AU - Peter Ruth AU - Gerd Geisslinger AU - Andreas Leffler AU - Robert Lukowski AU - Achim Schmidtko Y1 - 2015/01/21 UR - http://www.jneurosci.org/content/35/3/1125.abstract N2 - Slack (Slo2.2) is a sodium-activated potassium channel that regulates neuronal firing activities and patterns. Previous studies identified Slack in sensory neurons, but its contribution to acute and chronic pain in vivo remains elusive. Here we generated global and sensory neuron-specific Slack mutant mice and analyzed their behavior in various animal models of pain. Global ablation of Slack led to increased hypersensitivity in models of neuropathic pain, whereas the behavior in models of inflammatory and acute nociceptive pain was normal. Neuropathic pain behaviors were also exaggerated after ablation of Slack selectively in sensory neurons. Notably, the Slack opener loxapine ameliorated persisting neuropathic pain behaviors. In conclusion, Slack selectively controls the sensory input in neuropathic pain states, suggesting that modulating its activity might represent a novel strategy for management of neuropathic pain. ER -