Key result
Mutations in the SCN9A gene are associated with variations in pain sensitivity, ranging from complete insensitivity to extreme sensitivity.
Understanding SCN9A gene mutations and their effect on NaV1.7 channels is essential for developing targeted pain treatments.
SCN9A variants may inform perioperative pain management; leaves open targeted NaV1.7 modulation in practice.
Voltage-gated sodium channels (NaV) play a crucial role in development and propagation of action potentials in neurons and muscle cells. NaV1.7 channels take a special place in modern science since it is believed that they contribute to nerve hyperexcitability. Mutations of the gene SCN9A, which codes the α subunit of NaV1.7 channels, are associated with pain perception disorders (primary erythermalgia, congenital analgesia, and paroxysmal pain disorder). It is considered that the SCN9A gene mutations may cause variations in sensitivity to pain, from complete insensitivity to extreme sensitivity. Further research of the SCN9A gene polymorphism influence on pain sensitivity is essential for the understanding of the pathophysiology of pain and the development of the appropriate targeted pain treatment.
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Marković et al. (2015) conducted a review in Pain perception disorders. SCN9A gene mutations was evaluated on Pain sensitivity variations. Mutations in the SCN9A gene are associated with variations in pain sensitivity, ranging from complete insensitivity to extreme sensitivity.
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