This blog post is on the trail of potential new treatments for chronic pain conditions.
NaV1.8 is one of the types of voltage-gated sodium channels present in pain sensory neurons. Several types of ion channels have been associated with various kinds of pain sensation (1). There is interest in the idea that NaV1.8 is specialized for a role in the sensation of pain that can intensify after tissue damage and during inflammation.
There appears to be a NaV1.8-expressing population of sensory neurons that depends on the transcription factor Runx1 (2). These NaV1.8-expressing neurons carry inflammatory pain signals.
It has been suggested that signals associated with inflammation can recruit more NaV1.8 sodium channels to the cell membrane (3). There is also evidence that existing cell surface NaV1.8 channels can have their activity be regulated by phosphorylation, possibly making pain sensory neurons more active in response to signals produced during inflammation.
Given the role of NaV1.8 in pain sensation, there is interest in finding NaV1.8-specific inhibitors (4).
Image credits. Source. Some organisms make and accumulate toxins that bind to sodium channel proteins and alter their behavior.
Related blog. First step toward the holy grail of pain research?