Nociceptors—Noxious Stimulus Detectors

Nociception is essential for survival whereas pathological pain is maladaptive and often unresponsive to pharmacotherapy. Voltage-gated sodium channels, Na(v)1.1-Na(v)1.9, are essential for generation and conduction of electrical impulses in excitable cells. Human and animal studies have identified several channels as pivotal for signal transmission along the pain axis, including Na(v)1.3, Na(v)1.7, Na(v)1.8, and Na(v)1.9, with the latter three preferentially expressed in peripheral sensory neurons and Na(v)1.3 being upregulated along pain-signaling pathways after nervous system injuries. Na(v)1.7 is of special interest because it has been linked to a spectrum of inherited human pain disorders. Here we review the contribution of these sodium channel isoforms to pain.

Sodium Channels in Normal and Pathological Pain

Mutations in SCN9A, which encodes the voltage-gated sodium channel NaV1.7, can lead to severe neuropathic pain in humans. In this Review, Waxman and colleagues examine the mechanistic basis of NaV1.7-linked pain and explore strategies for targeting this channel in pain therapy.

The Na(V)1.7 sodium channel: from molecule to man.

Acute pain signaling has a key protective role and is highly evolutionarily conserved. Chronic pain, however, is maladaptive, occurring as a consequence of injury and disease, and is associated wit...

The Role of Voltage-Gated Sodium Channels in Pain Signaling

Burn injury: Challenges and advances in burn wound healing, infection, pain and scarring

Congenital indifference to pain (CIP) is a rare condition in which patients have severely impaired pain perception, but are otherwise essentially normal. We identified and collected DNA from individuals from nine families of seven different nationalities in which the affected individuals meet the diagnostic criteria for CIP. Using homozygosity mapping and haplotype sharing methods, we narrowed the CIP locus to chromosome 2q24-q31, a region known to contain a cluster of voltage-gated sodium channel genes. From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Na v 1.7. The mutations completely co-segregated with the disease phenotype, and nine of these SCN9A mutations resulted in truncation and loss-of-function of the Na v 1.7 channel. These genetic data further support the evidence that Na v 1.7 plays an essential role in mediating pain in humans, and that SCN9A mutations identified in multiple different populations underlie CIP.

Loss‐of‐function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations

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Loss‐of‐function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations