Journal
PARASITOLOGY
Volume 133, Issue -, Pages 67-74Publisher
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0031182006000023
Keywords
Schistosoma; calcium; contraction; calcium channel; calcium mobilization; dihydropyridines; thapsigargin
Categories
Funding
- NIAID NIH HHS [R01-AI49162] Funding Source: Medline
Ask authors/readers for more resources
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 mu M). 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. Furthermore, the contraction induced by 5 mM caffeine was inhibited after depletion of the sarcoplasmic reticulum either with thapsigargin (10 mu M) or ryanodine (10 mu M). These data suggest that voltage-operated Ca2+ channels docontribute to S. mansoni contraction as does the mobilization of stored Ca2+, despite the small volume of sarcoplasmic reticulum in schistosome smooth muscles.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available