Kv7.2 regulates the function of peripheral sensory neurons |
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Authors: | Chih H. King Eric Lancaster Daniela Salomon Elior Peles Steven S. Scherer |
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Affiliation: | 1. Department of Neuroscience, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania;2. Department of Neurology, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania;3. Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel |
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Abstract: | The Kv7 (KCNQ) family of voltage‐gated K+ channels regulates cellular excitability. The functional role of Kv7.2 has been hampered by the lack of a viable Kcnq2‐null animal model. In this study, we generated homozygous Kcnq2‐null sensory neurons using the Cre‐Lox system; in these mice, Kv7.2 expression is absent in the peripheral sensory neurons, whereas the expression of other molecular components of nodes (including Kv7.3), paranodes, and juxtaparanodes is not altered. The conditional Kcnq2‐null animals exhibit normal motor performance but have increased thermal hyperalgesia and mechanical allodynia. Whole‐cell patch recording technique demonstrates that Kcnq2‐null sensory neurons have increased excitability and reduced spike frequency adaptation. Taken together, our results suggest that the loss of Kv7.2 activity increases the excitability of primary sensory neurons. J. Comp. Neurol. 522:3262–3280, 2014. © 2014 Wiley Periodicals, Inc. |
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Keywords: | KCNQ M‐current dorsal root ganglion nociceptors Kv7 |
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