Loss-of-function mutations in sodium channel Nav1.7 cause anosmia

  title={Loss-of-function mutations in sodium channel Nav1.7 cause anosmia},
  author={Jan Weiss and Martina Pyrski and Eric Jacobi and Bernd Bufe and Vivienne Willnecker and Bernhard Schick and Philippe Zizzari and Samuel J. Gossage and Charles August Greer and Trese Leinders-Zufall and C Geoffrey Woods and John N Wood and Frank Zufall},
Loss of function of the gene SCN9A, encoding the voltage-gated sodium channel Nav1.7, causes a congenital inability to experience pain in humans. Here we show that Nav1.7 is not only necessary for pain sensation but is also an essential requirement for odour perception in both mice and humans. We examined human patients with loss-of-function mutations in SCN9A and show that they are unable to sense odours. To establish the essential role of Nav1.7 in odour perception, we generated conditional… CONTINUE READING
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Publications referenced by this paper.
Showing 1-10 of 42 references

Age-induced disruption of selective olfactory bulb synaptic circuits.

Proceedings of the National Academy of Sciences of the United States of America • 2010

mammalian odor perception

A. Keller, Vosshall, L. B. Better smelling through genetics
Curr. Opin. Neurobiol. 18, 364–369 • 2008

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