Invertebrate voltage-gated sodium channel (Nav)

Invertebrate voltage-gated sodium channels (Nav) are essential transmembrane proteins that mediate the rapid influx of sodium ions required for action potential generation and propagation in the invertebrate nervous system (Dong et al., 2014, DOI: 10.1016/j.ibmb.2014.01.001). In most insects, these channels are encoded by a single gene, typically named 'para', which undergoes extensive alternative splicing and RNA editing to generate functional diversity (Silver et al., 2014, DOI: 10.1016/j.pestbp.2014.03.003). These channels are the primary molecular targets for several major classes of insecticides, including pyrethroids, DDT, and oxadiazines (Zlotkin, 1999, DOI: 10.1016/S0065-308X(08)60151-3). Pyrethroids and DDT act by binding to specific sites on the channel to delay its inactivation, resulting in prolonged sodium currents, neuronal hyperexcitability, and eventual paralysis (Davies et al., 2007, DOI: 10.1016/j.pestbp.2007.01.007). In contrast, sodium channel blocker insecticides (SCBIs) like indoxacarb and metaflumizone inhibit the channel, leading to a loss of electrical activity (Silver et al., 2014). The development of resistance, particularly through knockdown resistance (kdr) mutations in the channel protein, remains a significant challenge in pest and vector control (Dong et al., 2014).

Other names

Insect voltage-gated sodium channelPara-type sodium channelVoltage-dependent sodium channelNav1-type channel

Modulation of channel gating kinetics by delaying inactivation or stabilizing the open state, or pore blockade to prevent sodium influx.