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.

Catherine 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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