Diversity of atrial local Ca2+ signalling: evidence from 2-D confocal imaging in Ca2+-buffered rat atrial myocytes
Atrial myocytes, lacking t-tubules, have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery colocalized with dihydropyridine receptors (DHPRs), and those at the cell interior not associated with DHPRs. We have previously shown that the Ca 2+ current ( I Ca )-gated...
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| description | Atrial myocytes, lacking t-tubules, have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery
colocalized with dihydropyridine receptors (DHPRs), and those at the cell interior not associated with DHPRs. We have previously
shown that the Ca 2+ current ( I Ca )-gated central Ca 2+ release has a fast component that is followed by a slower and delayed rising phase. The mechanisms that regulate the central
Ca 2+ releases remain poorly understood. The fast central release component is highly resistant to dialysed Ca 2+ buffers, while the slower, delayed component is completely suppressed by such exogenous buffers. Here we used dialysis of
Ca 2+ buffers (EGTA) into voltage-clamped rat atrial myocytes to isolate the fast component of central Ca 2+ release and examine its properties using rapid (240 Hz) two-dimensional confocal Ca 2+ imaging. We found two populations of rat atrial myocytes with respect to the ratio of central to peripheral Ca 2+ release ( R c/p ). In one population (âgroup 1â, â¼60% of cells), R c/p converged on 0.2, while in another population (âgroup 2â, â¼40%), R c/p had a Gaussian distribution with a mean value of 0.625. The fast central release component of group 2 cells appeared to result
from in-focus Ca 2+ sparks on activation of I Ca . In group 1 cells intracellular membranes associated with t-tubular structures were never seen using short exposures to membrane
dyes. In most of the group 2 cells, a faint intracellular membrane staining was observed. Quantification of caffeine-releasable
Ca 2+ pools consistently showed larger central Ca 2+ stores in group 2 and larger peripheral stores in group 1 cells. The R c/p was larger at more positive and negative voltages in group 1 cells. In contrast, in group 2 cells, the R c/p was constant at all voltages. In group 1 cells the gain of peripheral Ca 2+ release sites (Î[Ca 2+ ]/ I Ca ) was larger at â30 than at +20 mV, but significantly dampened at the central sites. On the other hand, the gains of peripheral
and central Ca 2+ releases in group 2 cells showed no voltage dependence. Surprisingly, the voltage dependence of the fast central release
component was bell-shaped and similar to that of I Ca in both cell groups. Removal of extracellular Ca 2+ or application of Ni 2+ (5 m m ) suppressed equally I Ca and Ca 2+ release from the central release sites at +60 mV. Depolarization to +100 mV, where I Ca is absent and the Na + âCa 2+ exchanger (NCX) act |
| doi_str_mv | 10.1113/jphysiol.2005.092270 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1474227</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68591636</sourcerecordid><originalsourceid>FETCH-LOGICAL-h3229-47faa386b0ede45fb6cf3dea9c394c5188d7d909535ed71f2000eb167feaea843</originalsourceid><addsrcrecordid>eNpVkUtv1DAUhS0EotPCP0DIK1igDH7EccyiEpqWlyrBoqwtx7meuHLiwc5MlX9Ppunw2NiL-51zr85B6BUla0opf3-366bsY1gzQsSaKMYkeYJWtKxUIaXiT9GKEMYKLgU9Q-c53xFCOVHqOTqjFWGkFGqF0pU_QMp-nHB02IzJm4BDtPO7Mewdzn47mBD8sP2A4eBbGCxgl2KPWXGFbRzcA-t7s50Z7IcHWdHsnYMELU5mPLn2U7TTCPkFeuZMyPDy8b9APz9d326-FDffP3_dfLwpOs6YKkrpjOF11RBooRSuqazjLRhluSqtoHXdylYRJbiAVlI3x0CgoZV0YMDUJb9Al4vvbt_00FoYxmSC3qX52DTpaLz-fzL4Tm_jQdNSlnOas8GbR4MUf-0hj7r32UIIZoC4z7qqhaIVr2bw9b-b_qw4xTwDagHufYDp75zoY5X6VKU-VqmXKvXttx-UkqP27aLt_La79wn0QudoPYyTFpXUXCsi-G-1b6Nn</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68591636</pqid></control><display><type>article</type><title>Diversity of atrial local Ca2+ signalling: evidence from 2-D confocal imaging in Ca2+-buffered rat atrial myocytes</title><source>MEDLINE</source><source>IngentaConnect Free/Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Wiley Online Library Free Content</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Woo, Sun‐Hee ; Cleemann, Lars ; Morad, Martin</creator><creatorcontrib>Woo, Sun‐Hee ; Cleemann, Lars ; Morad, Martin</creatorcontrib><description>Atrial myocytes, lacking t-tubules, have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery
colocalized with dihydropyridine receptors (DHPRs), and those at the cell interior not associated with DHPRs. We have previously
shown that the Ca 2+ current ( I Ca )-gated central Ca 2+ release has a fast component that is followed by a slower and delayed rising phase. The mechanisms that regulate the central
Ca 2+ releases remain poorly understood. The fast central release component is highly resistant to dialysed Ca 2+ buffers, while the slower, delayed component is completely suppressed by such exogenous buffers. Here we used dialysis of
Ca 2+ buffers (EGTA) into voltage-clamped rat atrial myocytes to isolate the fast component of central Ca 2+ release and examine its properties using rapid (240 Hz) two-dimensional confocal Ca 2+ imaging. We found two populations of rat atrial myocytes with respect to the ratio of central to peripheral Ca 2+ release ( R c/p ). In one population (âgroup 1â, â¼60% of cells), R c/p converged on 0.2, while in another population (âgroup 2â, â¼40%), R c/p had a Gaussian distribution with a mean value of 0.625. The fast central release component of group 2 cells appeared to result
from in-focus Ca 2+ sparks on activation of I Ca . In group 1 cells intracellular membranes associated with t-tubular structures were never seen using short exposures to membrane
dyes. In most of the group 2 cells, a faint intracellular membrane staining was observed. Quantification of caffeine-releasable
Ca 2+ pools consistently showed larger central Ca 2+ stores in group 2 and larger peripheral stores in group 1 cells. The R c/p was larger at more positive and negative voltages in group 1 cells. In contrast, in group 2 cells, the R c/p was constant at all voltages. In group 1 cells the gain of peripheral Ca 2+ release sites (Î[Ca 2+ ]/ I Ca ) was larger at â30 than at +20 mV, but significantly dampened at the central sites. On the other hand, the gains of peripheral
and central Ca 2+ releases in group 2 cells showed no voltage dependence. Surprisingly, the voltage dependence of the fast central release
component was bell-shaped and similar to that of I Ca in both cell groups. Removal of extracellular Ca 2+ or application of Ni 2+ (5 m m ) suppressed equally I Ca and Ca 2+ release from the central release sites at +60 mV. Depolarization to +100 mV, where I Ca is absent and the Na + âCa 2+ exchanger (NCX) acts in reverse mode, did not trigger the fast central Ca 2+ releases in either group, but brief reduction of [Na + ] o to levels equivalent to [Na + ] i facilitated fast peripheral and central Ca 2+ releases in group 2 myocytes, but not in group 1 myocytes. In group 2 cells, long-lasting (> 1 min) exposures to caffeine
(10 m m ) or ryanodine (20 μ m ) significantly suppressed I Ca -triggered central and peripheral Ca 2+ releases. Our data suggest significant diversity of local Ca 2+ signalling in rat atrial myocytes. In one group, I Ca -triggered peripheral Ca 2+ release propagates into the interior triggering central Ca 2+ release with significant delay. In a second group of myocytes I Ca triggers a significant number of central sites as rapidly and effectively as the peripheral sites, thereby producing more
synchronized Ca 2+ releases throughout the myocytes. The possible presence of vestigial t-tubules and larger Ca 2+ content of central sarcoplasmic reticulum (SR) in group 2 cells may be responsible for the rapid and strong activation of
central release of Ca 2+ in this subset of atrial myocytes.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2005.092270</identifier><identifier>PMID: 16020459</identifier><language>eng</language><publisher>9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society</publisher><subject>Aniline Compounds ; Animals ; Caffeine - pharmacology ; Calcium Channels, L-Type - metabolism ; Calcium Signaling - physiology ; Cell Physiology ; Fluorescent Dyes ; Heart Atria - metabolism ; In Vitro Techniques ; Male ; Membrane Potentials - physiology ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - physiology ; Pyridinium Compounds ; Rats ; Rats, Wistar ; Ryanodine - pharmacology ; Sarcoplasmic Reticulum - metabolism ; Xanthenes</subject><ispartof>The Journal of physiology, 2005-09, Vol.567 (3), p.905-921</ispartof><rights>2005 The Journal of Physiology © 2005 The Physiological Society</rights><rights>The Physiological society 2005 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1474227/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1474227/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16020459$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Woo, Sun‐Hee</creatorcontrib><creatorcontrib>Cleemann, Lars</creatorcontrib><creatorcontrib>Morad, Martin</creatorcontrib><title>Diversity of atrial local Ca2+ signalling: evidence from 2-D confocal imaging in Ca2+-buffered rat atrial myocytes</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Atrial myocytes, lacking t-tubules, have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery
colocalized with dihydropyridine receptors (DHPRs), and those at the cell interior not associated with DHPRs. We have previously
shown that the Ca 2+ current ( I Ca )-gated central Ca 2+ release has a fast component that is followed by a slower and delayed rising phase. The mechanisms that regulate the central
Ca 2+ releases remain poorly understood. The fast central release component is highly resistant to dialysed Ca 2+ buffers, while the slower, delayed component is completely suppressed by such exogenous buffers. Here we used dialysis of
Ca 2+ buffers (EGTA) into voltage-clamped rat atrial myocytes to isolate the fast component of central Ca 2+ release and examine its properties using rapid (240 Hz) two-dimensional confocal Ca 2+ imaging. We found two populations of rat atrial myocytes with respect to the ratio of central to peripheral Ca 2+ release ( R c/p ). In one population (âgroup 1â, â¼60% of cells), R c/p converged on 0.2, while in another population (âgroup 2â, â¼40%), R c/p had a Gaussian distribution with a mean value of 0.625. The fast central release component of group 2 cells appeared to result
from in-focus Ca 2+ sparks on activation of I Ca . In group 1 cells intracellular membranes associated with t-tubular structures were never seen using short exposures to membrane
dyes. In most of the group 2 cells, a faint intracellular membrane staining was observed. Quantification of caffeine-releasable
Ca 2+ pools consistently showed larger central Ca 2+ stores in group 2 and larger peripheral stores in group 1 cells. The R c/p was larger at more positive and negative voltages in group 1 cells. In contrast, in group 2 cells, the R c/p was constant at all voltages. In group 1 cells the gain of peripheral Ca 2+ release sites (Î[Ca 2+ ]/ I Ca ) was larger at â30 than at +20 mV, but significantly dampened at the central sites. On the other hand, the gains of peripheral
and central Ca 2+ releases in group 2 cells showed no voltage dependence. Surprisingly, the voltage dependence of the fast central release
component was bell-shaped and similar to that of I Ca in both cell groups. Removal of extracellular Ca 2+ or application of Ni 2+ (5 m m ) suppressed equally I Ca and Ca 2+ release from the central release sites at +60 mV. Depolarization to +100 mV, where I Ca is absent and the Na + âCa 2+ exchanger (NCX) acts in reverse mode, did not trigger the fast central Ca 2+ releases in either group, but brief reduction of [Na + ] o to levels equivalent to [Na + ] i facilitated fast peripheral and central Ca 2+ releases in group 2 myocytes, but not in group 1 myocytes. In group 2 cells, long-lasting (> 1 min) exposures to caffeine
(10 m m ) or ryanodine (20 μ m ) significantly suppressed I Ca -triggered central and peripheral Ca 2+ releases. Our data suggest significant diversity of local Ca 2+ signalling in rat atrial myocytes. In one group, I Ca -triggered peripheral Ca 2+ release propagates into the interior triggering central Ca 2+ release with significant delay. In a second group of myocytes I Ca triggers a significant number of central sites as rapidly and effectively as the peripheral sites, thereby producing more
synchronized Ca 2+ releases throughout the myocytes. The possible presence of vestigial t-tubules and larger Ca 2+ content of central sarcoplasmic reticulum (SR) in group 2 cells may be responsible for the rapid and strong activation of
central release of Ca 2+ in this subset of atrial myocytes.</description><subject>Aniline Compounds</subject><subject>Animals</subject><subject>Caffeine - pharmacology</subject><subject>Calcium Channels, L-Type - metabolism</subject><subject>Calcium Signaling - physiology</subject><subject>Cell Physiology</subject><subject>Fluorescent Dyes</subject><subject>Heart Atria - metabolism</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Membrane Potentials - physiology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Pyridinium Compounds</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Ryanodine - pharmacology</subject><subject>Sarcoplasmic Reticulum - metabolism</subject><subject>Xanthenes</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUtv1DAUhS0EotPCP0DIK1igDH7EccyiEpqWlyrBoqwtx7meuHLiwc5MlX9Ppunw2NiL-51zr85B6BUla0opf3-366bsY1gzQsSaKMYkeYJWtKxUIaXiT9GKEMYKLgU9Q-c53xFCOVHqOTqjFWGkFGqF0pU_QMp-nHB02IzJm4BDtPO7Mewdzn47mBD8sP2A4eBbGCxgl2KPWXGFbRzcA-t7s50Z7IcHWdHsnYMELU5mPLn2U7TTCPkFeuZMyPDy8b9APz9d326-FDffP3_dfLwpOs6YKkrpjOF11RBooRSuqazjLRhluSqtoHXdylYRJbiAVlI3x0CgoZV0YMDUJb9Al4vvbt_00FoYxmSC3qX52DTpaLz-fzL4Tm_jQdNSlnOas8GbR4MUf-0hj7r32UIIZoC4z7qqhaIVr2bw9b-b_qw4xTwDagHufYDp75zoY5X6VKU-VqmXKvXttx-UkqP27aLt_La79wn0QudoPYyTFpXUXCsi-G-1b6Nn</recordid><startdate>20050915</startdate><enddate>20050915</enddate><creator>Woo, Sun‐Hee</creator><creator>Cleemann, Lars</creator><creator>Morad, Martin</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Blackwell Science Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20050915</creationdate><title>Diversity of atrial local Ca2+ signalling: evidence from 2-D confocal imaging in Ca2+-buffered rat atrial myocytes</title><author>Woo, Sun‐Hee ; Cleemann, Lars ; Morad, Martin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h3229-47faa386b0ede45fb6cf3dea9c394c5188d7d909535ed71f2000eb167feaea843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aniline Compounds</topic><topic>Animals</topic><topic>Caffeine - pharmacology</topic><topic>Calcium Channels, L-Type - metabolism</topic><topic>Calcium Signaling - physiology</topic><topic>Cell Physiology</topic><topic>Fluorescent Dyes</topic><topic>Heart Atria - metabolism</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Membrane Potentials - physiology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Pyridinium Compounds</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Ryanodine - pharmacology</topic><topic>Sarcoplasmic Reticulum - metabolism</topic><topic>Xanthenes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Woo, Sun‐Hee</creatorcontrib><creatorcontrib>Cleemann, Lars</creatorcontrib><creatorcontrib>Morad, Martin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Woo, Sun‐Hee</au><au>Cleemann, Lars</au><au>Morad, Martin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diversity of atrial local Ca2+ signalling: evidence from 2-D confocal imaging in Ca2+-buffered rat atrial myocytes</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2005-09-15</date><risdate>2005</risdate><volume>567</volume><issue>3</issue><spage>905</spage><epage>921</epage><pages>905-921</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>Atrial myocytes, lacking t-tubules, have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery
colocalized with dihydropyridine receptors (DHPRs), and those at the cell interior not associated with DHPRs. We have previously
shown that the Ca 2+ current ( I Ca )-gated central Ca 2+ release has a fast component that is followed by a slower and delayed rising phase. The mechanisms that regulate the central
Ca 2+ releases remain poorly understood. The fast central release component is highly resistant to dialysed Ca 2+ buffers, while the slower, delayed component is completely suppressed by such exogenous buffers. Here we used dialysis of
Ca 2+ buffers (EGTA) into voltage-clamped rat atrial myocytes to isolate the fast component of central Ca 2+ release and examine its properties using rapid (240 Hz) two-dimensional confocal Ca 2+ imaging. We found two populations of rat atrial myocytes with respect to the ratio of central to peripheral Ca 2+ release ( R c/p ). In one population (âgroup 1â, â¼60% of cells), R c/p converged on 0.2, while in another population (âgroup 2â, â¼40%), R c/p had a Gaussian distribution with a mean value of 0.625. The fast central release component of group 2 cells appeared to result
from in-focus Ca 2+ sparks on activation of I Ca . In group 1 cells intracellular membranes associated with t-tubular structures were never seen using short exposures to membrane
dyes. In most of the group 2 cells, a faint intracellular membrane staining was observed. Quantification of caffeine-releasable
Ca 2+ pools consistently showed larger central Ca 2+ stores in group 2 and larger peripheral stores in group 1 cells. The R c/p was larger at more positive and negative voltages in group 1 cells. In contrast, in group 2 cells, the R c/p was constant at all voltages. In group 1 cells the gain of peripheral Ca 2+ release sites (Î[Ca 2+ ]/ I Ca ) was larger at â30 than at +20 mV, but significantly dampened at the central sites. On the other hand, the gains of peripheral
and central Ca 2+ releases in group 2 cells showed no voltage dependence. Surprisingly, the voltage dependence of the fast central release
component was bell-shaped and similar to that of I Ca in both cell groups. Removal of extracellular Ca 2+ or application of Ni 2+ (5 m m ) suppressed equally I Ca and Ca 2+ release from the central release sites at +60 mV. Depolarization to +100 mV, where I Ca is absent and the Na + âCa 2+ exchanger (NCX) acts in reverse mode, did not trigger the fast central Ca 2+ releases in either group, but brief reduction of [Na + ] o to levels equivalent to [Na + ] i facilitated fast peripheral and central Ca 2+ releases in group 2 myocytes, but not in group 1 myocytes. In group 2 cells, long-lasting (> 1 min) exposures to caffeine
(10 m m ) or ryanodine (20 μ m ) significantly suppressed I Ca -triggered central and peripheral Ca 2+ releases. Our data suggest significant diversity of local Ca 2+ signalling in rat atrial myocytes. In one group, I Ca -triggered peripheral Ca 2+ release propagates into the interior triggering central Ca 2+ release with significant delay. In a second group of myocytes I Ca triggers a significant number of central sites as rapidly and effectively as the peripheral sites, thereby producing more
synchronized Ca 2+ releases throughout the myocytes. The possible presence of vestigial t-tubules and larger Ca 2+ content of central sarcoplasmic reticulum (SR) in group 2 cells may be responsible for the rapid and strong activation of
central release of Ca 2+ in this subset of atrial myocytes.</abstract><cop>9600 Garsington Road , Oxford , OX4 2DQ , UK</cop><pub>The Physiological Society</pub><pmid>16020459</pmid><doi>10.1113/jphysiol.2005.092270</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; IngentaConnect Free/Open Access Journals; Wiley Online Library Journals Frontfile Complete; Wiley Online Library Free Content; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Aniline Compounds Animals Caffeine - pharmacology Calcium Channels, L-Type - metabolism Calcium Signaling - physiology Cell Physiology Fluorescent Dyes Heart Atria - metabolism In Vitro Techniques Male Membrane Potentials - physiology Myocytes, Cardiac - metabolism Myocytes, Cardiac - physiology Pyridinium Compounds Rats Rats, Wistar Ryanodine - pharmacology Sarcoplasmic Reticulum - metabolism Xanthenes |
| title | Diversity of atrial local Ca2+ signalling: evidence from 2-D confocal imaging in Ca2+-buffered rat atrial myocytes |
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