2015
DOI: 10.1523/jneurosci.2423-14.2015
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Slack Channels Expressed in Sensory Neurons Control Neuropathic Pain in Mice

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 acut… Show more

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Cited by 73 publications
(149 citation statements)
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“…The absence of any motor coordination deficits is in line with our previous study showing that lack of Slack does not affect the performance on an accelerating rotarod (Lu et al 2015).…”
Section: Slack-deficient Mice Show Normal Motor Functionssupporting
confidence: 92%
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“…The absence of any motor coordination deficits is in line with our previous study showing that lack of Slack does not affect the performance on an accelerating rotarod (Lu et al 2015).…”
Section: Slack-deficient Mice Show Normal Motor Functionssupporting
confidence: 92%
“…Since most of the tests studying unconditioned anxiety largely depend on normal explorative behavior and locomotion, it is presently difficult for us to estimate the impact of endogenous Slack channels in regulating anxiety by studying our global Slack mutant mouse model. Future studies on tissue-specific Slack KOs that show a normal explorative behavior but selectively lack Slack channels in brain regions involved in anxiety-related neuronal circuits (e.g., the amygdala or the prefrontal cortex) will be required to adequately address this issue (Lu et al 2015).…”
Section: Discussionmentioning
confidence: 99%
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“…The channel is also expressed at high levels in nociceptive neurons within the dorsal root ganglion, and suppression of current using several approaches, including deletion of the gene for K Na 1.1, enhances neuronal excitability and produces hypersensitivity of animals to several pain-inducing stimuli (Gao et al, 2008;Tamsett et al, 2009;Nuwer et al, 2010;Huang et al, 2013;Lu et al, 2015;Martinez-Espinosa et al, 2015). Deletion of the gene in mice also has a variety of more wide-ranging effects on behavior, including an inability to reverse a previously learned behavior (Bausch et al, 2015).…”
Section: The K Ca 2 Family-small Conductance Channels Regulated mentioning
confidence: 99%