Parasitic worm voltage-gated calcium channel

Parasitic worm calcium channels, most notably *voltage-gated calcium channels* (Ca_v), are membrane protein complexes involved in mediating the influx of extracellular calcium ions in response to membrane depolarization. These channels are critical for *muscle contraction*, *motility*, and other physiological functions in adult parasitic worms such as schistosomes (causative agents of schistosomiasis)[5][4][3]. The pore-forming \u03b1_1 subunit is modulated by unique auxiliary subunits in schistosomes, and some flatworms possess novel channel subtypes like TRPM_{PZQ}, which is directly targeted and activated by praziquantel therapy, leading to sustained calcium entry and worm paralysis[3][4]. Drug resistance has emerged as a therapeutic issue due to genetic variants in the TRPM_{PZQ} binding pocket[3]. Other compounds, such as nifedipine (a general L-type Ca_v channel blocker), have demonstrated efficacy against worm calcium channels, supporting their utility as validated drug targets[2][5]. **Note:** The name "Parasitic worm calcium channels" is *not a canonical full name*\u2014it represents an entire class of channels rather than a specific molecular entity. For most drug targeting purposes, the more precise name would be "Schistosoma mansoni transient receptor potential melastatin ion channel (TRPM_{PZQ})" or "Schistosoma mansoni voltage-gated calcium channel," depending on target specificity[3][4][5][7]. The current entry is overly broad and should be refined for structured use. **Correction (is_incorrect flag):** The target name "Parasitic worm calcium channels" is overly generic and combines multiple related but distinct ion channel types, some of which are only partially characterized or may not be targeted directly by available drugs[3][4][5][7]. For accurate structured information, the target should be specified to the protein subtype most relevant to drug action\u2014for example, *TRPM_{PZQ}* for schistosome praziquantel sensitivity[3], or voltage-gated Ca_v channel in specific nematodes or flatworms[5][7][4].

Other names

Parasitic worm Ca(^{2+}) channelFlatworm voltage-gated calcium channelSchistosome Ca(^{2+}) channelVoltage-operated calcium channel (VOCC) (parasite-specific context)

*Praziquantel:* Activates TRPM_{PZQ} channels, causes sustained Ca^{2+} influx and muscular paralysis of the worm, leading to death[3][4][5]. *Nifedipine:* Blocks L-type Ca^{2+} channels, disrupting Ca^{2+} homeostasis and causing worm motility impairment and death[2][5]. *Emodepside:* Activates SLO-1 (BK-type Ca^{2+}-activated K^{+} channels) in nematodes, not directly on Ca^{2+} channels but functionally related[4][8].