Physiology and pharmacology of flatworm muscle

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dc.contributor.advisor Timothy A. Day
dc.contributor.advisor Walter H. Hsu
dc.contributor.advisor Douglas E. Jones
dc.contributor.author Novozhilova, Ekaterina
dc.contributor.department Theses & dissertations (Interdisciplinary)
dc.date 2018-08-22T17:04:13.000
dc.date.accessioned 2020-06-30T07:46:48Z
dc.date.available 2020-06-30T07:46:48Z
dc.date.copyright Tue Jan 01 00:00:00 UTC 2008
dc.date.issued 2008-01-01
dc.description.abstract <p>Pharmacological characterization of voltage-operated Ca2+ channels (VOCCs), in both free-living and parasitic flatworms, has been difficult since the currents carried by these channels are small in amplitude and run down quickly. While the presence of VOCCs in the parasite Schistosoma mansoni has been evident from molecular data, they have escaped pharmacological characterization. In this study, we have been able to consistently record inward currents carried by VOCCs in isolated S. mansoni muscle fibers, using whole cell configuration of the patch-clamp technique in voltage-clamp mode. Inward voltage-activated current was recorded, under conditions that suppressed outward K+ conductance, by the replacement of internal K+ with Cs+ and enhanced with 15.0 mM Ba 2+ as a charge carrier in addition to 2.0 mM Ca2+ (I Ca/Ba). Whole cell ICa/Ba was obtained from frayed muscle fibers by depolarizing them for 200 ms from a holding potential of -70 mV to +20 mV. A relatively small proportion of cells tested (less than 30%) had currents with amplitudes amenable to pharmacological characterization using common VOCCs blockers and neuropeptides. Currents showed little evidence of inactivation within the period of the 200 ms depolarizing pulse. Currents were sensitive to the phenylalkylamine VOCC blocker verapamil, which reduced their amplitude in concentration-dependent manner. The platyhelminth-derived FMRFamide-like peptide (FLP) YIRFamide significantly increased current amplitude at 1muM. YIRFamide's ability to amplify the inward currents was reduced when verapamil was simultaneously present in the perfusion solution, indicating possible VOCCs involvement in carrying Ca2+ influx triggered by the flatworm FLP.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/rtd/15732/
dc.identifier.articleid 16731
dc.identifier.contextkey 7042958
dc.identifier.doi https://doi.org/10.31274/rtd-180813-16940
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath rtd/15732
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/69394
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/rtd/15732/3323718.PDF|||Fri Jan 14 20:45:50 UTC 2022
dc.subject.disciplines Animal Sciences
dc.subject.disciplines Neuroscience and Neurobiology
dc.subject.disciplines Neurosciences
dc.subject.disciplines Parasitology
dc.subject.disciplines Physiology
dc.subject.disciplines Veterinary Physiology
dc.subject.keywords Biomedical sciences;Neuroscience
dc.title Physiology and pharmacology of flatworm muscle
dc.type article
dc.type.genre dissertation
dspace.entity.type Publication
thesis.degree.discipline Neuroscience
thesis.degree.level dissertation
thesis.degree.name Doctor of Philosophy
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