Preventing postsurgical pain
Opiate abuse has necessitated finding alternative therapeutic targets to alleviate postsurgical pain. The Ca2+ channel CaV3.2 has been implicated in inflammatory and neuropathic pain. Joksimovic et al. now show that postsurgical pain also triggers CaV3.2 channel activity by increasing its stability at the surface of pain-sensing neurons. In rodents, pharmacologically inhibiting CaV3.2 or preventing the deubiquitinating enzyme USP5 from stabilizing the channel reversed postoperative hypersensitivity to mechanical and heat stimuli, pain syndromes that are also typical in patients after surgery. Targeting CaV3.2 or the ability of USP5 to bind to the channel may provide a strategy for relieving postsurgical pain that lacks the addiction potential of opiates.
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