Transient receptor potential channel (filarial worm)

Transient receptor potential (TRP) channels in filarial worms are a diverse family of non-selective cation channels, including TRPC-like, TRPV-like, TRPM-like, and TRPA-like subtypes, that mediate sensory and contractile functions by controlling calcium entry and membrane potential in worm neurons and muscle[1][4][5][9]. These channels play key roles in sensory signal transduction, muscle contraction, and overall worm movement. The anti-filarial drug diethylcarbamazine directly activates several of these channels—particularly TRP-2 (a TRPC-like subtype), GON-2, and CED-11 (TRPM-like subtypes)—leading to rapid, temporary spastic paralysis of the worms by inducing calcium influx in muscle cells[4][5][9]. TRP channels are essential for the viability and motility of filarial parasites and are considered validated therapeutic targets for nematode infections such as lymphatic filariasis and loiasis[4][5][9]. The functional conservation of these channels among nematodes highlights the potential for species-selective or broad-spectrum anthelmintic drug development targeting TRP channels[1][4][5].

Other names

TRP channel (filarial worm)Filarial TRP channelTRP-2 (filarial worm)OSM-9 (filarial worm)OCR-1 (filarial worm)GON-2 (filarial worm)CED-11 (filarial worm)TRPA-2 (filarial worm)

Activation of TRP channels in filarial muscle, leading to Ca(2+) influx, membrane depolarization, and spastic paralysis of the worm[4][5][9].