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 a2c1
a1 Departamento de Farmacologia Básica e Clínica, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Brazil
a2 Department of Biomedical Sciences, Iowa State University, Ames, IA 50011, USA
a3 Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48854, USA
a4 Parasitology Research Group, The Queen's University of Belfast, Belfast, Northern Ireland, UK

Article author query
mendonca-silva dl   [PubMed][Google Scholar] 
novozhilova e   [PubMed][Google Scholar] 
cobbett pj   [PubMed][Google Scholar] 
silva cl   [PubMed][Google Scholar] 
noel f   [PubMed][Google Scholar] 
totten mi   [PubMed][Google Scholar] 
maule ag   [PubMed][Google Scholar] 
day ta   [PubMed][Google Scholar] 


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.

(Received October 11 2005)
(Revised December 22 2005)
(Accepted December 23 2005)
(Published Online March 28 2006)

Key Words: Schistosoma; calcium; contraction; calcium channel; calcium mobilization; dihydropyridines; thapsigargin.

c1 Department of Biomedical Sciences, Iowa State University, Ames, IA 50011, USA. Tel: +515 294 7100. Fax: +515 294 2315. E-mail: