Calcitonin Gene-Related Peptide Enhances the Rate of Desensitization of the Nicotinic Acetylcholine Receptor in Cultured Mouse Muscle Cells
Calcitonin gene-related peptide (CGRP) is a neuropeptide that coexists with acetylcholine in spinal cord motoneurons. The effects of CGRP on the functional properties of the nicotinic acetylcholine receptor (AcChoR) were examined by electrophysiological methods. Using the whole-cell patch-clamp tech...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1988-08, Vol.85 (15), p.5728-5732 |
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| creator | Mulle, Christophe Benoit, Pierre Pinset, Christian Roa, Michèle Changeux, Jean-Pierre |
| description | Calcitonin gene-related peptide (CGRP) is a neuropeptide that coexists with acetylcholine in spinal cord motoneurons. The effects of CGRP on the functional properties of the nicotinic acetylcholine receptor (AcChoR) were examined by electrophysiological methods. Using the whole-cell patch-clamp technique and a mouse cell line derived from soleus muscle, we found that CGRP produces a progressive and reversible enhancement of the rapid-decay phase of AcChoR desensitization. Single-channel data further show that CGRP decreases acetylcholine-activated channel opening frequency. This decrease occurs when CGRP and acetylcholine are applied on different cell-surface areas and thus is likely mediated by a second-messenger system. CGRP is also shown to increase cAMP accumulation in this cell line. The effects of CGRP on macroscopic acetylcholine-activated currents are mimicked by external application of forskolin (10 μ M) or by internal perfusion of the cell with cAMP (1 mM). In both these cases, further application of CGRP produces no additional enhancement of AcChoR desensitization. These results suggest that, on mouse muscle cells, CGRP regulates AcChoR desensitization by a mechanism that involves, at least in part, cAMP-dependent phosphorylation of the AcChoR. |
| doi_str_mv | 10.1073/pnas.85.15.5728 |
| format | Article |
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The effects of CGRP on the functional properties of the nicotinic acetylcholine receptor (AcChoR) were examined by electrophysiological methods. Using the whole-cell patch-clamp technique and a mouse cell line derived from soleus muscle, we found that CGRP produces a progressive and reversible enhancement of the rapid-decay phase of AcChoR desensitization. Single-channel data further show that CGRP decreases acetylcholine-activated channel opening frequency. This decrease occurs when CGRP and acetylcholine are applied on different cell-surface areas and thus is likely mediated by a second-messenger system. CGRP is also shown to increase cAMP accumulation in this cell line. The effects of CGRP on macroscopic acetylcholine-activated currents are mimicked by external application of forskolin (10 μ M) or by internal perfusion of the cell with cAMP (1 mM). In both these cases, further application of CGRP produces no additional enhancement of AcChoR desensitization. These results suggest that, on mouse muscle cells, CGRP regulates AcChoR desensitization by a mechanism that involves, at least in part, cAMP-dependent phosphorylation of the AcChoR.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.85.15.5728</identifier><identifier>PMID: 2456580</identifier><identifier>CODEN: PNASA6</identifier><language>eng</language><publisher>Washington, DC: National Academy of Sciences of the United States of America</publisher><subject>acetylcholine ; Animals ; Biological and medical sciences ; Calcitonin - genetics ; Calcitonin Gene-Related Peptide ; Calcium - metabolism ; Cell lines ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Clone Cells ; Colforsin - pharmacology ; Cyclic AMP - metabolism ; Electrophysiology ; Fundamental and applied biological sciences. Psychology ; Inurement ; Ion Channels - drug effects ; Mice ; Mice, Inbred C3H ; Muscle cells ; Muscle fibers ; muscles ; Muscles - cytology ; Muscles - metabolism ; Neuropeptides - pharmacology ; Nicotinic receptors ; Perfusion ; Phosphorylation ; Pipettes ; Receptors, Cholinergic - drug effects ; Receptors, Cholinergic - metabolism ; Synapses ; Time constants ; Vertebrates: nervous system and sense organs</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1988-08, Vol.85 (15), p.5728-5732</ispartof><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-13b6e86dfb2e07b55577c5d2a56cb66c4e71550c74f994bb9cd445530b62472c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/85/15.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/32229$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/32229$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7208458$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2456580$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mulle, Christophe</creatorcontrib><creatorcontrib>Benoit, Pierre</creatorcontrib><creatorcontrib>Pinset, Christian</creatorcontrib><creatorcontrib>Roa, Michèle</creatorcontrib><creatorcontrib>Changeux, Jean-Pierre</creatorcontrib><title>Calcitonin Gene-Related Peptide Enhances the Rate of Desensitization of the Nicotinic Acetylcholine Receptor in Cultured Mouse Muscle Cells</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Calcitonin gene-related peptide (CGRP) is a neuropeptide that coexists with acetylcholine in spinal cord motoneurons. The effects of CGRP on the functional properties of the nicotinic acetylcholine receptor (AcChoR) were examined by electrophysiological methods. Using the whole-cell patch-clamp technique and a mouse cell line derived from soleus muscle, we found that CGRP produces a progressive and reversible enhancement of the rapid-decay phase of AcChoR desensitization. Single-channel data further show that CGRP decreases acetylcholine-activated channel opening frequency. This decrease occurs when CGRP and acetylcholine are applied on different cell-surface areas and thus is likely mediated by a second-messenger system. CGRP is also shown to increase cAMP accumulation in this cell line. The effects of CGRP on macroscopic acetylcholine-activated currents are mimicked by external application of forskolin (10 μ M) or by internal perfusion of the cell with cAMP (1 mM). In both these cases, further application of CGRP produces no additional enhancement of AcChoR desensitization. These results suggest that, on mouse muscle cells, CGRP regulates AcChoR desensitization by a mechanism that involves, at least in part, cAMP-dependent phosphorylation of the AcChoR.</description><subject>acetylcholine</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcitonin - genetics</subject><subject>Calcitonin Gene-Related Peptide</subject><subject>Calcium - metabolism</subject><subject>Cell lines</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Clone Cells</subject><subject>Colforsin - pharmacology</subject><subject>Cyclic AMP - metabolism</subject><subject>Electrophysiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Inurement</subject><subject>Ion Channels - drug effects</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Muscle cells</subject><subject>Muscle fibers</subject><subject>muscles</subject><subject>Muscles - cytology</subject><subject>Muscles - metabolism</subject><subject>Neuropeptides - pharmacology</subject><subject>Nicotinic receptors</subject><subject>Perfusion</subject><subject>Phosphorylation</subject><subject>Pipettes</subject><subject>Receptors, Cholinergic - drug effects</subject><subject>Receptors, Cholinergic - metabolism</subject><subject>Synapses</subject><subject>Time constants</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAQhS0EKtvCGQkJ5AOCU7aO47GdYxVKQWoBVXCOHGeideV1ltiRKH-hfxpHu6zEBU4e-X3z3kiPkBclW5dMVee7YOJaw7qENSiuH5FVyeqykKJmj8mKMa4KLbh4Sk5jvGOM1aDZCTnhAmSeVuShMd66NAYX6BUGLG7Rm4Q9_Yq75Hqkl2FjgsVI0wbpbZboOND3GDFEl9wvk9wYlq9F_uzsmFxwll5YTPfebkbvQl5Dm93GieaQZvZpnnLAzThHpDdztB5pg97HZ-TJYHzE54f3jHz_cPmt-Vhcf7n61FxcFxaqKhVl1UnUsh86jkx1AKCUhZ4bkLaT0gpUJQCzSgx1Lbqutr0QABXrJBeK2-qMvN377qbxx4wxtVsXbb7ABMxHtUpXXHKp_guWwLTUEjJ4vgftNMY44dDuJrc1031bsnbpqV16ajXklXbpKW-8OljP3Rb7I38oJutvDrqJ1vhhyiW4eMQUZ1rAYvP6gC3-f9S_ct79E2iH2fuEP1MmX-7Ju5irOqIV57yufgMx5r1J</recordid><startdate>19880801</startdate><enddate>19880801</enddate><creator>Mulle, Christophe</creator><creator>Benoit, Pierre</creator><creator>Pinset, Christian</creator><creator>Roa, Michèle</creator><creator>Changeux, Jean-Pierre</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19880801</creationdate><title>Calcitonin Gene-Related Peptide Enhances the Rate of Desensitization of the Nicotinic Acetylcholine Receptor in Cultured Mouse Muscle Cells</title><author>Mulle, Christophe ; Benoit, Pierre ; Pinset, Christian ; Roa, Michèle ; Changeux, Jean-Pierre</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-13b6e86dfb2e07b55577c5d2a56cb66c4e71550c74f994bb9cd445530b62472c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>acetylcholine</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcitonin - genetics</topic><topic>Calcitonin Gene-Related Peptide</topic><topic>Calcium - metabolism</topic><topic>Cell lines</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Clone Cells</topic><topic>Colforsin - pharmacology</topic><topic>Cyclic AMP - metabolism</topic><topic>Electrophysiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Inurement</topic><topic>Ion Channels - drug effects</topic><topic>Mice</topic><topic>Mice, Inbred C3H</topic><topic>Muscle cells</topic><topic>Muscle fibers</topic><topic>muscles</topic><topic>Muscles - cytology</topic><topic>Muscles - metabolism</topic><topic>Neuropeptides - pharmacology</topic><topic>Nicotinic receptors</topic><topic>Perfusion</topic><topic>Phosphorylation</topic><topic>Pipettes</topic><topic>Receptors, Cholinergic - drug effects</topic><topic>Receptors, Cholinergic - metabolism</topic><topic>Synapses</topic><topic>Time constants</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mulle, Christophe</creatorcontrib><creatorcontrib>Benoit, Pierre</creatorcontrib><creatorcontrib>Pinset, Christian</creatorcontrib><creatorcontrib>Roa, Michèle</creatorcontrib><creatorcontrib>Changeux, Jean-Pierre</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mulle, Christophe</au><au>Benoit, Pierre</au><au>Pinset, Christian</au><au>Roa, Michèle</au><au>Changeux, Jean-Pierre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcitonin Gene-Related Peptide Enhances the Rate of Desensitization of the Nicotinic Acetylcholine Receptor in Cultured Mouse Muscle Cells</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1988-08-01</date><risdate>1988</risdate><volume>85</volume><issue>15</issue><spage>5728</spage><epage>5732</epage><pages>5728-5732</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><coden>PNASA6</coden><abstract>Calcitonin gene-related peptide (CGRP) is a neuropeptide that coexists with acetylcholine in spinal cord motoneurons. The effects of CGRP on the functional properties of the nicotinic acetylcholine receptor (AcChoR) were examined by electrophysiological methods. Using the whole-cell patch-clamp technique and a mouse cell line derived from soleus muscle, we found that CGRP produces a progressive and reversible enhancement of the rapid-decay phase of AcChoR desensitization. Single-channel data further show that CGRP decreases acetylcholine-activated channel opening frequency. This decrease occurs when CGRP and acetylcholine are applied on different cell-surface areas and thus is likely mediated by a second-messenger system. CGRP is also shown to increase cAMP accumulation in this cell line. The effects of CGRP on macroscopic acetylcholine-activated currents are mimicked by external application of forskolin (10 μ M) or by internal perfusion of the cell with cAMP (1 mM). In both these cases, further application of CGRP produces no additional enhancement of AcChoR desensitization. These results suggest that, on mouse muscle cells, CGRP regulates AcChoR desensitization by a mechanism that involves, at least in part, cAMP-dependent phosphorylation of the AcChoR.</abstract><cop>Washington, DC</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>2456580</pmid><doi>10.1073/pnas.85.15.5728</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 1988-08, Vol.85 (15), p.5728-5732 |
| issn | 0027-8424 1091-6490 |
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| recordid | cdi_pnas_primary_85_15_5728 |
| source | Jstor Complete Legacy; MEDLINE; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | acetylcholine Animals Biological and medical sciences Calcitonin - genetics Calcitonin Gene-Related Peptide Calcium - metabolism Cell lines Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Clone Cells Colforsin - pharmacology Cyclic AMP - metabolism Electrophysiology Fundamental and applied biological sciences. Psychology Inurement Ion Channels - drug effects Mice Mice, Inbred C3H Muscle cells Muscle fibers muscles Muscles - cytology Muscles - metabolism Neuropeptides - pharmacology Nicotinic receptors Perfusion Phosphorylation Pipettes Receptors, Cholinergic - drug effects Receptors, Cholinergic - metabolism Synapses Time constants Vertebrates: nervous system and sense organs |
| title | Calcitonin Gene-Related Peptide Enhances the Rate of Desensitization of the Nicotinic Acetylcholine Receptor in Cultured Mouse Muscle Cells |
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