File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Local control models of cardiac excitation-contraction coupling: A possible role for allosteric interactions between ryanodine receptors

TitleLocal control models of cardiac excitation-contraction coupling: A possible role for allosteric interactions between ryanodine receptors
Authors
KeywordsCalcium-induced calcium release
Diad junction
Dihydropyridine receptor
Monte Carlo
Sarcoplasmic reticulum
Issue Date1999
Citation
Journal of General Physiology, 1999, v. 113 n. 3, p. 469-489 How to Cite?
AbstractIn cardiac muscle, release of activator calcium from the sarcoplasmic reticulum occurs by calcium-induced calcium release through ryanodine receptors (RyRs), which are clustered in a dense, regular, two-dimensional lattice array at the diad junction. We simulated numerically the stochastic dynamics of RyRs and L-type sarcolemmal calcium channels interacting via calcium nano-domains in the junctional cleft. Four putative RyR gating schemes based on single-channel measurements in lipid bilayers all failed to give stable excitation-contraction coupling, due either to insufficiently strong inactivation to terminate locally regenerative calcium-induced calcium release or insufficient cooperativity to discriminate against RyR activation by background calcium. If the ryanodine receptor was represented, instead, by a phenomenological four-state gating scheme, with channel opening resulting from simultaneous binding of two Ca2+ ions, and either calcium-dependent or activation-linked inactivation, the simulations gave a good semiquantitative accounting for the macroscopic features of excitation-contraction coupling. It was possible to restore stability to a model based on a bilayer-derived gating scheme, by introducing allosteric interactions between nearest- neighbor RyRs so as to stabilize the inactivated state and produce cooperativity among calcium binding sites on different RyRs. Such allosteric coupling between RyRs may be a function of the foot process and lattice array, explaining their conservation during evolution.
Persistent Identifierhttp://hdl.handle.net/10722/195155
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 1.270
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorStern, MD-
dc.contributor.authorSong, L-S-
dc.contributor.authorCheng, H-
dc.contributor.authorSham, JSK-
dc.contributor.authorYang, HT-
dc.contributor.authorBoheler, KR-
dc.contributor.authorRíos, E-
dc.date.accessioned2014-02-25T01:40:14Z-
dc.date.available2014-02-25T01:40:14Z-
dc.date.issued1999-
dc.identifier.citationJournal of General Physiology, 1999, v. 113 n. 3, p. 469-489-
dc.identifier.issn0022-1295-
dc.identifier.urihttp://hdl.handle.net/10722/195155-
dc.description.abstractIn cardiac muscle, release of activator calcium from the sarcoplasmic reticulum occurs by calcium-induced calcium release through ryanodine receptors (RyRs), which are clustered in a dense, regular, two-dimensional lattice array at the diad junction. We simulated numerically the stochastic dynamics of RyRs and L-type sarcolemmal calcium channels interacting via calcium nano-domains in the junctional cleft. Four putative RyR gating schemes based on single-channel measurements in lipid bilayers all failed to give stable excitation-contraction coupling, due either to insufficiently strong inactivation to terminate locally regenerative calcium-induced calcium release or insufficient cooperativity to discriminate against RyR activation by background calcium. If the ryanodine receptor was represented, instead, by a phenomenological four-state gating scheme, with channel opening resulting from simultaneous binding of two Ca2+ ions, and either calcium-dependent or activation-linked inactivation, the simulations gave a good semiquantitative accounting for the macroscopic features of excitation-contraction coupling. It was possible to restore stability to a model based on a bilayer-derived gating scheme, by introducing allosteric interactions between nearest- neighbor RyRs so as to stabilize the inactivated state and produce cooperativity among calcium binding sites on different RyRs. Such allosteric coupling between RyRs may be a function of the foot process and lattice array, explaining their conservation during evolution.-
dc.languageeng-
dc.relation.ispartofJournal of General Physiology-
dc.subjectCalcium-induced calcium release-
dc.subjectDiad junction-
dc.subjectDihydropyridine receptor-
dc.subjectMonte Carlo-
dc.subjectSarcoplasmic reticulum-
dc.titleLocal control models of cardiac excitation-contraction coupling: A possible role for allosteric interactions between ryanodine receptors-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1085/jgp.113.3.469-
dc.identifier.pmid10051521-
dc.identifier.scopuseid_2-s2.0-0032949168-
dc.identifier.volume113-
dc.identifier.issue3-
dc.identifier.spage469-
dc.identifier.epage489-
dc.identifier.isiWOS:000078967700011-
dc.identifier.issnl0022-1295-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats