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L-type Ca2+ channel and ryanodine receptor cross-talk in frog skeletal muscle
The dihydropyridine receptors (DHPRs) /L -type Ca 2+ channels of skeletal muscle are coupled with ryanodine receptors/Ca 2+ release channels (RyRs/CRCs) located in the sarcoplasmic reticulum (SR). The DHPR is the voltage sensor for excitationâcontraction (EC) coupling and the charge movement compo...
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Published in: | The Journal of physiology 2004-02, Vol.555 (1), p.137-152 |
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creator | Squecco, Roberta Bencini, Chiara Piperio, Claudia Francini, Fabio |
description | The dihydropyridine receptors (DHPRs) /L -type Ca 2+ channels of skeletal muscle are coupled with ryanodine receptors/Ca 2+ release channels (RyRs/CRCs) located in the sarcoplasmic reticulum (SR). The DHPR is the voltage sensor for excitationâcontraction
(EC) coupling and the charge movement component q γ has been implicated as the signal linking DHPR voltage sensing to Ca 2+ release from the coupled RyR. Recently, a new charge component, q h , has been described and related to L- type Ca 2+ channel gating. Evidence has also been provided that the coupled RyR/CRC can modulate DHPR functions via a retrograde signal.
Our aim was to investigate whether the newly described q h is also involved in the reciprocal interaction or cross-talk between DHPR/ L- type Ca 2+ channel and RyR/CRC. To this end we interfered with DHPR/ L- type Ca 2+ channel function using nifedipine and 1-alkanols (heptanol and octanol), and with RyR/CRC function using ryanodine and ruthenium
red (RR). Intramembrane charge movement (ICM) and L- type Ca 2+ current ( I Ca ) were measured in single cut fibres of the frog using the double-Vaseline-gap technique. Our records showed that nifedipine
reduced the amount of q γ and q h moved by â¼90% and â¼55%, respectively, whereas 1-alkanols completely abolished them. Ryanodine and RR shifted the transition
voltages of q γ and q h and of the maximal conductance of I Ca by â¼4â9 mV towards positive potentials. All these interventions spared q β . These results support the hypothesis that only q γ ; and q h arise from the movement of charged particles within the DHPR/ L- type Ca 2+ channel and that these charge components together with I Ca are affected by a retrograde signal from RyR/CRC. |
doi_str_mv | 10.1113/jphysiol.2003.051730 |
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(EC) coupling and the charge movement component q γ has been implicated as the signal linking DHPR voltage sensing to Ca 2+ release from the coupled RyR. Recently, a new charge component, q h , has been described and related to L- type Ca 2+ channel gating. Evidence has also been provided that the coupled RyR/CRC can modulate DHPR functions via a retrograde signal.
Our aim was to investigate whether the newly described q h is also involved in the reciprocal interaction or cross-talk between DHPR/ L- type Ca 2+ channel and RyR/CRC. To this end we interfered with DHPR/ L- type Ca 2+ channel function using nifedipine and 1-alkanols (heptanol and octanol), and with RyR/CRC function using ryanodine and ruthenium
red (RR). Intramembrane charge movement (ICM) and L- type Ca 2+ current ( I Ca ) were measured in single cut fibres of the frog using the double-Vaseline-gap technique. Our records showed that nifedipine
reduced the amount of q γ and q h moved by â¼90% and â¼55%, respectively, whereas 1-alkanols completely abolished them. Ryanodine and RR shifted the transition
voltages of q γ and q h and of the maximal conductance of I Ca by â¼4â9 mV towards positive potentials. All these interventions spared q β . These results support the hypothesis that only q γ ; and q h arise from the movement of charged particles within the DHPR/ L- type Ca 2+ channel and that these charge components together with I Ca are affected by a retrograde signal from RyR/CRC.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2003.051730</identifier><identifier>PMID: 14660705</identifier><language>eng</language><publisher>9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society</publisher><subject>Animals ; Calcium Channels, L-Type - physiology ; In Vitro Techniques ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - physiology ; Nifedipine - pharmacology ; Rana esculenta ; Receptor Cross-Talk - drug effects ; Receptor Cross-Talk - physiology ; Research Papers ; Ryanodine Receptor Calcium Release Channel - physiology</subject><ispartof>The Journal of physiology, 2004-02, Vol.555 (1), p.137-152</ispartof><rights>2004 The Journal of Physiology © 2004 The Physiological Society</rights><rights>The Physiological Society 2003 2003</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/PMC1664826/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664826/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14660705$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Squecco, Roberta</creatorcontrib><creatorcontrib>Bencini, Chiara</creatorcontrib><creatorcontrib>Piperio, Claudia</creatorcontrib><creatorcontrib>Francini, Fabio</creatorcontrib><title>L-type Ca2+ channel and ryanodine receptor cross-talk in frog skeletal muscle</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>The dihydropyridine receptors (DHPRs) /L -type Ca 2+ channels of skeletal muscle are coupled with ryanodine receptors/Ca 2+ release channels (RyRs/CRCs) located in the sarcoplasmic reticulum (SR). The DHPR is the voltage sensor for excitationâcontraction
(EC) coupling and the charge movement component q γ has been implicated as the signal linking DHPR voltage sensing to Ca 2+ release from the coupled RyR. Recently, a new charge component, q h , has been described and related to L- type Ca 2+ channel gating. Evidence has also been provided that the coupled RyR/CRC can modulate DHPR functions via a retrograde signal.
Our aim was to investigate whether the newly described q h is also involved in the reciprocal interaction or cross-talk between DHPR/ L- type Ca 2+ channel and RyR/CRC. To this end we interfered with DHPR/ L- type Ca 2+ channel function using nifedipine and 1-alkanols (heptanol and octanol), and with RyR/CRC function using ryanodine and ruthenium
red (RR). Intramembrane charge movement (ICM) and L- type Ca 2+ current ( I Ca ) were measured in single cut fibres of the frog using the double-Vaseline-gap technique. Our records showed that nifedipine
reduced the amount of q γ and q h moved by â¼90% and â¼55%, respectively, whereas 1-alkanols completely abolished them. Ryanodine and RR shifted the transition
voltages of q γ and q h and of the maximal conductance of I Ca by â¼4â9 mV towards positive potentials. All these interventions spared q β . These results support the hypothesis that only q γ ; and q h arise from the movement of charged particles within the DHPR/ L- type Ca 2+ channel and that these charge components together with I Ca are affected by a retrograde signal from RyR/CRC.</description><subject>Animals</subject><subject>Calcium Channels, L-Type - physiology</subject><subject>In Vitro Techniques</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - physiology</subject><subject>Nifedipine - pharmacology</subject><subject>Rana esculenta</subject><subject>Receptor Cross-Talk - drug effects</subject><subject>Receptor Cross-Talk - physiology</subject><subject>Research Papers</subject><subject>Ryanodine Receptor Calcium Release Channel - physiology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNpVkVtv1DAQhS0EokvhHyDkJ3iosnjs9SUvSGhFuWgRPJRny3FmN269cbCzVPn3pErL5WmkOd-cI80h5CWwNQCIt9dDN5WQ4pozJtZMghbsEVnBRtWV1rV4TFaMcV4JLeGMPCvlmjEQrK6fkrMZUkwzuSJfd9U4DUi3jl9Q37m-x0hd39I8uT61oUea0eMwpkx9TqVUo4s3NPR0n9OBlhuMOG_o8VR8xOfkyd7Fgi_u5zn5cfnhavup2n37-Hn7fld1wmhR1UIZROMbI73kjAND4I1pwOh51WwaWTdtXXsu9b71TAtunDISQAnFfdOKc_Ju8R1OzRFbj_2YXbRDDkeXJ5tcsP8rfejsIf2yoNTGcDUbvL43yOnnCctoj6F4jNH1mE7FGgbK6I2ZwVf_Jv2JePjgDJgFuA0Rp786s3ct2YeW7F1LdmnJXn35DkzMp2-W0y4cutuQ0S5wST7gOFkppQULQovfShCVJQ</recordid><startdate>20040215</startdate><enddate>20040215</enddate><creator>Squecco, Roberta</creator><creator>Bencini, Chiara</creator><creator>Piperio, Claudia</creator><creator>Francini, Fabio</creator><general>The Physiological Society</general><general>Blackwell Publishing 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>20040215</creationdate><title>L-type Ca2+ channel and ryanodine receptor cross-talk in frog skeletal muscle</title><author>Squecco, Roberta ; Bencini, Chiara ; Piperio, Claudia ; Francini, Fabio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h3873-9368ee8cb85c520210e12b8b187b85b4b59bd99c257fdc07328a685116362cbd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Calcium Channels, L-Type - physiology</topic><topic>In Vitro Techniques</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscle, Skeletal - physiology</topic><topic>Nifedipine - pharmacology</topic><topic>Rana esculenta</topic><topic>Receptor Cross-Talk - drug effects</topic><topic>Receptor Cross-Talk - physiology</topic><topic>Research Papers</topic><topic>Ryanodine Receptor Calcium Release Channel - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Squecco, Roberta</creatorcontrib><creatorcontrib>Bencini, Chiara</creatorcontrib><creatorcontrib>Piperio, Claudia</creatorcontrib><creatorcontrib>Francini, Fabio</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>Squecco, Roberta</au><au>Bencini, Chiara</au><au>Piperio, Claudia</au><au>Francini, Fabio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>L-type Ca2+ channel and ryanodine receptor cross-talk in frog skeletal muscle</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2004-02-15</date><risdate>2004</risdate><volume>555</volume><issue>1</issue><spage>137</spage><epage>152</epage><pages>137-152</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>The dihydropyridine receptors (DHPRs) /L -type Ca 2+ channels of skeletal muscle are coupled with ryanodine receptors/Ca 2+ release channels (RyRs/CRCs) located in the sarcoplasmic reticulum (SR). The DHPR is the voltage sensor for excitationâcontraction
(EC) coupling and the charge movement component q γ has been implicated as the signal linking DHPR voltage sensing to Ca 2+ release from the coupled RyR. Recently, a new charge component, q h , has been described and related to L- type Ca 2+ channel gating. Evidence has also been provided that the coupled RyR/CRC can modulate DHPR functions via a retrograde signal.
Our aim was to investigate whether the newly described q h is also involved in the reciprocal interaction or cross-talk between DHPR/ L- type Ca 2+ channel and RyR/CRC. To this end we interfered with DHPR/ L- type Ca 2+ channel function using nifedipine and 1-alkanols (heptanol and octanol), and with RyR/CRC function using ryanodine and ruthenium
red (RR). Intramembrane charge movement (ICM) and L- type Ca 2+ current ( I Ca ) were measured in single cut fibres of the frog using the double-Vaseline-gap technique. Our records showed that nifedipine
reduced the amount of q γ and q h moved by â¼90% and â¼55%, respectively, whereas 1-alkanols completely abolished them. Ryanodine and RR shifted the transition
voltages of q γ and q h and of the maximal conductance of I Ca by â¼4â9 mV towards positive potentials. All these interventions spared q β . These results support the hypothesis that only q γ ; and q h arise from the movement of charged particles within the DHPR/ L- type Ca 2+ channel and that these charge components together with I Ca are affected by a retrograde signal from RyR/CRC.</abstract><cop>9600 Garsington Road , Oxford , OX4 2DQ , UK</cop><pub>The Physiological Society</pub><pmid>14660705</pmid><doi>10.1113/jphysiol.2003.051730</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Calcium Channels, L-Type - physiology In Vitro Techniques Muscle, Skeletal - drug effects Muscle, Skeletal - physiology Nifedipine - pharmacology Rana esculenta Receptor Cross-Talk - drug effects Receptor Cross-Talk - physiology Research Papers Ryanodine Receptor Calcium Release Channel - physiology |
title | L-type Ca2+ channel and ryanodine receptor cross-talk in frog skeletal muscle |
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