Referenced in: none

Automatically associated channels: Slo1 , Slo2

Title: Slack channels expressed in sensory neurons control neuropathic pain in mice.

Authors: Ruirui Lu, Anne E Bausch, Wiebke Kallenborn-Gerhardt, Carsten Stoetzer, Natasja Debruin, Peter Ruth, Gerd Geisslinger, Andreas Leffler, Robert Lukowski, Achim Schmidtko

Journal, date & volume: J. Neurosci., 2015 Jan 21 , 35, 1125-35

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25609627

Abstract
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.