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 …

The voltage-gated sodium channel NaV1. 7 is preferentially expressed in peripheral somatic
and visceral sensory neurons, olfactory sensory neurons and sympathetic ganglion neurons …

Nociception is essential for survival whereas pathological pain is maladaptive and often
unresponsive to pharmacotherapy. Voltage-gated sodium channels, Nav1. 1–Nav1. 9, are …

Pathogenic variants in the voltage-gated sodium channel gene family lead to early onset
epilepsies, neurodevelopmental disorders, skeletal muscle channelopathies, peripheral …

The activity of voltage-gated sodium channels has long been linked to disorders of neuronal
excitability such as epilepsy and chronic pain. Recent genetic studies have now expanded …

The discovery of genetic variants that substantially alter an individual's perception of pain
has led to a step-change in our understanding of molecular events underlying the detection …

The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause
a complete absence of pain, whereas activating mutations cause severe episodic pain in …

In the human genome more than 400 genes encode ion channels, which are
transmembrane proteins mediating ion fluxes across membranes. Being expressed in all …

Human studies have firmly implicated voltage-gated sodium channels in human pain
disorders, and targeted and massively parallel genomic sequencing is beginning to be used …

Voltage-gated sodium (Nav) channels are essential for the rapid upstroke of action
potentials and the propagation of electrical signals in nerves and muscles. Defects of Nav …