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Role of calcium influx through voltage-operated calcium channels and of calcium mobilization in the physiology of Schistosoma mansoni muscle contractions

  • D. L. MENDONÇA-SILVA (a1), E. NOVOZHILOVA (a2), P. J. R. COBBETT (a3), C. L. M. SILVA (a1), F. NOËL (a1), M. I. J. TOTTEN (a4), A. G. MAULE (a4) and T. A. DAY (a2)
  • DOI:
  • Published online: 28 March 2006

We tested the hypothesis that voltage-operated Ca2+ channels mediate an extracellular Ca2+ influx in muscle fibres from the human parasite Schistosoma mansoni and, along with Ca2+ mobilization from the sarcoplasmic reticulum, contribute to muscle contraction. Indeed, whole-cell voltage clamp revealed voltage-gated inward currents carried by divalent ions with a peak current elicited by steps to +20 mV (from a holding potential of −70 mV). Depolarization of the fibres by elevated extracellular K+ elicited contractions that were completely dependent on extracellular Ca2+ and inhibited by nicardipine (half inhibition at 4·1 μM). However these contractions were not very sensitive to other classical blockers of voltage-gated Ca2+ channels, indicating that the schistosome muscle channels have an atypical pharmacology when compared to their mammalian counterparts. Futhermore, the contraction induced by 5 mM caffeine was inhibited after depletion of the sarcoplasmic reticulum either with thapsigargin (10 μM) or ryanodine (10 μM). These data suggest that voltage-operated Ca2+ channels do contribute to S. mansoni contraction as does the mobilization of stored Ca2+, despite the small volume of sarcoplasmic reticulum in schistosome smooth muscles.

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Department of Biomedical Sciences, Iowa State University, Ames, IA 50011, USA. Tel: +515 294 7100. Fax: +515 294 2315. E-mail:
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  • ISSN: 0031-1820
  • EISSN: 1469-8161
  • URL: /core/journals/parasitology
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