| G protein-mediated FMRFamidergic modulation of calcium influx in dissociated heart muscle cells from squid, Loligo forbesii. | |
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MedLine Citation:
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PMID: 10835048 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The actions of the neuropeptide FMRFamide (Phe-Met-Arg-Phe-NH2) on the L-type (ICa,L) and T-type (ICa,T) calcium currents were investigated in muscle cells dissociated from the heart of squid, Loligo forbseii. The heart muscle cells could be divided into type I and type II cells, on the basis of morphological differences in the dissociated myocytes. FMRFamide induced a substantial block of the L-type calcium current seen in type I cells; this inhibition was rapid, reversible and dose dependent (IC50 = 0.1 microM). FMRFamide induced an increase in the amplitude of the L-type calcium current in the type II heart muscle cells, but had no effect on the T-type calcium current in either type of dissociated heart muscle cell, even at concentrations much higher than those found to affect the L-type calcium current. Internal dialysis of isolated type I heart muscle cells with guanosine 5'-O-(3-thiotriphosphate (GTPgammaS, 100 microM), a non-hydrolysable GTP analogue, mimicked the FMRFamide inhibition of the Ca2+ current and occluded any further FMRFamide-induced inhibition. Internal dialysis of these cells with guanosine 5'-O-(2-thiodiphosphate) (GDPbetaS, 100 microM) reduced the FMRFamide-induced inhibition of the peak Ca2+ current. The inhibitory effects of FMRFamide were abolished by pre-incubation of the cells with pertussis toxin (200 ng ml-1). The activation kinetics of ICa,L were not affected by FMRFamide application, nor by internal perfusion with GTPgammaS, and the FMRFamide-induced reduction in ICa,L was not relieved by large depolarising prepulses. These data indicate that FMRFamide can modulate ICa,L, but not ICa,T, in squid heart muscle cells, and that the underlying G protein pathway is dissimilar to that commonly associated with transmitter modulation of channel activity. The FMRFamide-modulated increase in ICa,L seen in the type II heart muscle cells was not mediated by a PTX-sensitive G protein pathway. |
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Authors:
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A Chrachri; M Odblom; R Williamson |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of physiology Volume: 525 Pt 2 ISSN: 0022-3751 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 2000 Jun |
Date Detail:
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Created Date: 2000-08-28 Completed Date: 2000-08-28 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 471-82 Citation Subset: IM |
Affiliation:
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Marine Biological Association of the UK, Citadel Hill, Plymouth PL1 2PB and Department of Biology, University of Plymouth, Plymouth PL4 8AA, UK. aacc@wpo.nerc.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Calcium / metabolism* Calcium Channels, L-Type / drug effects, metabolism Calcium Channels, T-Type / drug effects, metabolism Cell Separation Decapodiformes / cytology, metabolism* FMRFamide / pharmacology* GTP-Binding Proteins / metabolism* Guanosine 5'-O-(3-Thiotriphosphate) / pharmacology Guanosine Diphosphate / analogs & derivatives, pharmacology Kinetics Membrane Potentials Myocardium / cytology, metabolism* Pertussis Toxin Thionucleotides / pharmacology Virulence Factors, Bordetella / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channels, L-Type; 0/Calcium Channels, T-Type; 0/Thionucleotides; 0/Virulence Factors, Bordetella; 146-91-8/Guanosine Diphosphate; 37589-80-3/Guanosine 5'-O-(3-Thiotriphosphate); 64190-70-1/FMRFamide; 71376-97-1/guanosine 5'-O-(2-thiodiphosphate); 7440-70-2/Calcium; EC 2.4.2.31/Pertussis Toxin; EC 3.6.1.-/GTP-Binding Proteins |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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