Research ArticlePain

Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia

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Science Translational Medicine  20 Apr 2016:
Vol. 8, Issue 335, pp. 335ra56
DOI: 10.1126/scitranslmed.aad7653

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A gain in pain control

Subtype-specific blockade of sodium channel Nav1.7, which is important for firing of peripheral pain-signaling neurons, is a major focus of pain research. In a new study, Cao et al. created iPSC-derived sensory neurons from patients with inherited erythromelalgia (IEM), a painful disorder in which gain-of-function Nav1.7 mutations produce hyperexcitability and hyperresponsiveness to warmth in peripheral sensory neurons. The investigators show that a new selective Nav1.7 sodium channel blocker normalized the phenotype of iPSC-derived sensory neurons carrying IEM mutations and blocked pain perception in human subjects with IEM. These results provide proof of principle that selective Nav1.7 blockade may be useful in pain alleviation.

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