File Download
  Links for fulltext
     (May Require Subscription)

Conference Paper: A Neuromuscular Junction-like Calcium Release Mechanism In A Unicellular Organism

TitleA Neuromuscular Junction-like Calcium Release Mechanism In A Unicellular Organism
Authors
Issue Date2006
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
The 25th Scientific Meeting of the Hong Kong Society of Neurosciences (HKSN 2005), Hong Kong, December 2005. In NeuroSignals, 2006, v. 15 n. 3, p. 153-154, abstract P-29/25 How to Cite?
AbstractWhen a myocyte is depolarized by an action potential, calcium ions enter the cell through L-type calcium channels located on the sarcolemma. This calcium, or the physical interaction between the activated L-type calcium channel, triggers a subsequent release of calcium that is stored in the sarcoplasmic reticulum (SR) through calcium-release channels ryanodine receptors. Crypthecodium cohnii is an unicellular dinoflagellate (phyloge-netically related to malarial parasite) with cortical multi-membranous structures apparently similar to the SR. In the present study, both fluorescence-conjugated ryanodine and dihydropyridine gave positive labellings on the cortical area of dinoflagellate cells in where the chlortetracycline-stained calcium stores were located. Either mechanical stimulations or potassium ions could induce membrane potential changes and calcium mobilizations. In addition, cytosolic calcium mobilizations induced by L-type calcium channel agonist (Bay K) was inhibited by ryanodine receptor antagonist (dantrolene). When the membrane potentials were disrupted by sodium ionophore, both mechanically-induced cytosolic calcium mobilizations and membrane potential changes were reduced. This indicated that the dihydropyridine receptor-like protein was upstream of the ryanodine receptor-like channel. Accumulated data, therefore, are consistent with a neuromuscular type excitation-contraction coupling-like mechanism in the dinoflagellates. Acknowledgement: Part of this research was supported by HKUST’s EHIA05/06.SC04 in Molecular Medicine awarded to J.T.Y.W. and S.Y.W.S).
Descriptionpp. 111–156 of this Free journal issue entitled: Abstracts of the 24th and the 25th Scientific Meeting of the Hong Kong
Poster Presentations: no. P-29/25
Persistent Identifierhttp://hdl.handle.net/10722/105165
ISSN
2015 Impact Factor: 1.593
2015 SCImago Journal Rankings: 0.763

 

DC FieldValueLanguage
dc.contributor.authorYeung, PKKen_HK
dc.contributor.authorLam, CMCen_HK
dc.contributor.authorShiu, SYWen_HK
dc.contributor.authorWong, JTYen_HK
dc.date.accessioned2010-09-25T22:22:50Z-
dc.date.available2010-09-25T22:22:50Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 25th Scientific Meeting of the Hong Kong Society of Neurosciences (HKSN 2005), Hong Kong, December 2005. In NeuroSignals, 2006, v. 15 n. 3, p. 153-154, abstract P-29/25en_HK
dc.identifier.issn1424-862Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/105165-
dc.descriptionpp. 111–156 of this Free journal issue entitled: Abstracts of the 24th and the 25th Scientific Meeting of the Hong Kong-
dc.descriptionPoster Presentations: no. P-29/25-
dc.description.abstractWhen a myocyte is depolarized by an action potential, calcium ions enter the cell through L-type calcium channels located on the sarcolemma. This calcium, or the physical interaction between the activated L-type calcium channel, triggers a subsequent release of calcium that is stored in the sarcoplasmic reticulum (SR) through calcium-release channels ryanodine receptors. Crypthecodium cohnii is an unicellular dinoflagellate (phyloge-netically related to malarial parasite) with cortical multi-membranous structures apparently similar to the SR. In the present study, both fluorescence-conjugated ryanodine and dihydropyridine gave positive labellings on the cortical area of dinoflagellate cells in where the chlortetracycline-stained calcium stores were located. Either mechanical stimulations or potassium ions could induce membrane potential changes and calcium mobilizations. In addition, cytosolic calcium mobilizations induced by L-type calcium channel agonist (Bay K) was inhibited by ryanodine receptor antagonist (dantrolene). When the membrane potentials were disrupted by sodium ionophore, both mechanically-induced cytosolic calcium mobilizations and membrane potential changes were reduced. This indicated that the dihydropyridine receptor-like protein was upstream of the ryanodine receptor-like channel. Accumulated data, therefore, are consistent with a neuromuscular type excitation-contraction coupling-like mechanism in the dinoflagellates. Acknowledgement: Part of this research was supported by HKUST’s EHIA05/06.SC04 in Molecular Medicine awarded to J.T.Y.W. and S.Y.W.S).-
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_HK
dc.relation.ispartofNeuroSignalsen_HK
dc.rightsNeuroSignals. Copyright © S Karger AG.en_HK
dc.titleA Neuromuscular Junction-like Calcium Release Mechanism In A Unicellular Organismen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1424-862X&volume=15&spage=153&epage=154&date=2006&atitle=A+Neuromuscular+Junction-like+Calcium+Release+Mechanism+In+A+Unicellular+Organismen_HK
dc.identifier.emailShiu, SYW: sywshiu@hkucc.hku.hken_HK
dc.identifier.authorityShiu, SYW=rp00384en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1159/000095356-
dc.identifier.hkuros120712en_HK
dc.identifier.volume15en_HK
dc.identifier.issue3-
dc.identifier.spage153, abstract P-29/25-
dc.identifier.epage154en_HK
dc.identifier.epage154-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats