Loss of function of sodium channel Na1.7 produces pain insensitivity. In this issue, Deng et al. show that analgesia after Na1.7 removal or pharmacological blockade is not driven by enkephalin overexpression. These results underscore the essential role, independent of endogenous opioids, of Na1.7 for nociceptor firing and pain.
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| http://dx.doi.org/10.1016/j.neuron.2023.08.011 | DOI Listing |
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