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Sodium Channel

Voltage-gated sodium channels initiate action potentials in neurons and other excitable cells, and their dysfunction causes inherited epilepsy, chronic pain, and other diseases of hyperexcitability. Many of the basic functional properties of sodium channels were analyzed in extensive voltage clamp studies of nerve axons. [Na+] is known to be strictly controlled at 135 to 145 mM in the serum and cerebrospinal fluid (CSF) of mammals, including humans, which suggests that brain sensor(s) can detect an increase in [Na+] in this range in order to strictly maintain physiological levels. Voltage-gated sodium (NaV) channels are key transmembrane proteins that permit influx of Na+ in excitable and non-excitable cells where they contribute to setting the membrane potential, action potential initiation and propagation, as well as cell motility and proliferation. While NaV channels can be found in many tissues and cell types, they are particularly important for the function of central and peripheral neurons as well as skeletal and cardiac muscle. Seven NaV channels NaV1.1, NaV1.2, NaV1.3, NaV1.6, NaV1.7, NaV1.8, and NaV1.9 play major roles in electrogenesis in neurons. The Nax channel (also known as NaG or NaV2.1, in humans encoded by the gene SCN7A) also belongs to the family of the voltage-gated sodium channels, even though it is not activated by changes in membrane potential. Instead it is activated by an increased extracellular Na+ concentration and is involved in sodium level sensing in the central nervous system, in controlling salt intake behaviour as well as in regulating epithelial sodium homeostasis.

References

1.Catterall WA. Neurochem Res. 2017;42(9):2495–2504.
2.Deuis JR,et al. Neuropharmacology. 2017;127:87–108.

Membrane Transporter/Ion Channel

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