Infographic: A Painful Pathway

Since the mid-2000s, the voltage-gated sodium channel NaV1.7 has emerged as a promising target for a new class of analgesics.

Written byCatherine Offord

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Na_V1.7 controls the passage of sodium ions into sensory neurons. Hyperactivity in Na_V1.7 is associated with increased firing in pain-sensing neurons—and thus agony even in the absence of painful stimuli—while deletion of the channel appears to cause pain insensitivity.

© THOM GRAVESLike other voltage-gated sodium channels, Na_V1.7 consists of four voltage-sensing domains (I to IV) surrounding a central pore through which sodium ions pass into the neuron. As a sensory neuron fires (from left to right), voltage-gated sodium channels cycle through three states: from closed to open, and finally inactivated.

INACTIVATED
For a short period following opening, the voltage-sensing domains remain open, but the pore is blocked by a positively charged particle in a ball-and-chain mechanism.

OPEN
Voltage-sensing domains open during an action potential to allow sodium ions to flow into the neuron.

CLOSED
Voltage-sensing domains pinch shut the pore when the neuron is at rest.

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Meet the Author

Catherine Offord
After undergraduate research with spiders at the University of Oxford and graduate research with ants at Princeton University, Catherine left arthropods and academia to become a science journalist. She has worked in various guises at The Scientist since 2016. As Senior Editor, she wrote articles for the online and print publications, and edited the magazine’s Notebook, Careers, and Bio Business sections. She reports on subjects ranging from cellular and molecular biology to research misconduct and science policy. Find more of her work at her website.
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