Acetylcholine regulation of nicotinic receptor channels through a putative G protein in chick myotubes

1. Single-channel currents induced by acetylcholine (ACh) were recorded from unstriated and non-innervated embryonic chick myotubes using the cell-attached patch-clamp technique. 2. ACh applied to the non-patched membrane decreased both channel opening probability and conductance. These ACh-induced...

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Veröffentlicht in:The Journal of physiology 1987-12, Vol.393 (1), p.635-645
Hauptverfasser: Eusebi, F, Grassi, F, Molinaro, M, Zani, B M
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Grassi, F
Molinaro, M
Zani, B M
description 1. Single-channel currents induced by acetylcholine (ACh) were recorded from unstriated and non-innervated embryonic chick myotubes using the cell-attached patch-clamp technique. 2. ACh applied to the non-patched membrane decreased both channel opening probability and conductance. These ACh-induced effects occurred also when the non-patched membrane was exposed to nominally Ca2+-free extracellular medium, but were absent when it was treated with curare. 3. ACh-induced membrane current recorded under whole-cell patch-clamp conditions decreased in amplitude and time course when myotubes were intracellularly loaded with guanosine-5'-O-(3-thiotriphosphate) GTP gamma S), but not with guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) or cyclic adenosine-5'-monophosphate (cyclic AMP). Internal perfusion of GTP gamma S affected the ACh-induced openings in a similar manner to the non-patch ACh application. 4. These results suggest that ACh, in addition to its direct effect, acts indirectly on the nicotinic receptor channels by delivering an intracellular messenger and through the activation of a putative G protein.
doi_str_mv 10.1113/jphysiol.1987.sp016845
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Single-channel currents induced by acetylcholine (ACh) were recorded from unstriated and non-innervated embryonic chick myotubes using the cell-attached patch-clamp technique. 2. ACh applied to the non-patched membrane decreased both channel opening probability and conductance. These ACh-induced effects occurred also when the non-patched membrane was exposed to nominally Ca2+-free extracellular medium, but were absent when it was treated with curare. 3. ACh-induced membrane current recorded under whole-cell patch-clamp conditions decreased in amplitude and time course when myotubes were intracellularly loaded with guanosine-5'-O-(3-thiotriphosphate) GTP gamma S), but not with guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) or cyclic adenosine-5'-monophosphate (cyclic AMP). Internal perfusion of GTP gamma S affected the ACh-induced openings in a similar manner to the non-patch ACh application. 4. These results suggest that ACh, in addition to its direct effect, acts indirectly on the nicotinic receptor channels by delivering an intracellular messenger and through the activation of a putative G protein.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1987.sp016845</identifier><identifier>PMID: 2451747</identifier><identifier>CODEN: JPHYA7</identifier><language>eng</language><publisher>Oxford: The Physiological Society</publisher><subject>acetylcholine ; Acetylcholine - pharmacology ; Action Potentials - drug effects ; Animals ; Biological and medical sciences ; Calcium - pharmacology ; Cells, Cultured ; Chick Embryo ; Cyclic AMP - pharmacology ; Embryology: invertebrates and vertebrates. Teratology ; Experimental organogenesis ; Fundamental and applied biological sciences. Psychology ; guanine nucleotide-binding proteins ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Diphosphate - analogs &amp; derivatives ; Guanosine Diphosphate - pharmacology ; Guanosine Triphosphate - analogs &amp; derivatives ; Guanosine Triphosphate - pharmacology ; Ion Channels - drug effects ; membrane currents ; Muscles - embryology ; Muscles - physiology ; Nerve Tissue Proteins - physiology ; Organogenesis. 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Single-channel currents induced by acetylcholine (ACh) were recorded from unstriated and non-innervated embryonic chick myotubes using the cell-attached patch-clamp technique. 2. ACh applied to the non-patched membrane decreased both channel opening probability and conductance. These ACh-induced effects occurred also when the non-patched membrane was exposed to nominally Ca2+-free extracellular medium, but were absent when it was treated with curare. 3. ACh-induced membrane current recorded under whole-cell patch-clamp conditions decreased in amplitude and time course when myotubes were intracellularly loaded with guanosine-5'-O-(3-thiotriphosphate) GTP gamma S), but not with guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) or cyclic adenosine-5'-monophosphate (cyclic AMP). Internal perfusion of GTP gamma S affected the ACh-induced openings in a similar manner to the non-patch ACh application. 4. These results suggest that ACh, in addition to its direct effect, acts indirectly on the nicotinic receptor channels by delivering an intracellular messenger and through the activation of a putative G protein.</description><subject>acetylcholine</subject><subject>Acetylcholine - pharmacology</subject><subject>Action Potentials - drug effects</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - pharmacology</subject><subject>Cells, Cultured</subject><subject>Chick Embryo</subject><subject>Cyclic AMP - pharmacology</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Experimental organogenesis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>guanine nucleotide-binding proteins</subject><subject>Guanosine 5'-O-(3-Thiotriphosphate)</subject><subject>Guanosine Diphosphate - analogs &amp; derivatives</subject><subject>Guanosine Diphosphate - pharmacology</subject><subject>Guanosine Triphosphate - analogs &amp; derivatives</subject><subject>Guanosine Triphosphate - pharmacology</subject><subject>Ion Channels - drug effects</subject><subject>membrane currents</subject><subject>Muscles - embryology</subject><subject>Muscles - physiology</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Organogenesis. Physiological fonctions</subject><subject>Receptors, Nicotinic - physiology</subject><subject>skeletal muscle</subject><subject>Thionucleotides - pharmacology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkl9vFCEUxSdGU2v1I2h4MOrLrlz-Li8mtdGqaaIP9ZkAw-xQ2WGEmTb77WWz242-qAmB5N7fOVxyaJoXgJcAQN_ejP22hBSXoFZyWUYMYsX4g-YUmFALKRV92JxiTMiCSg6Pmyel3GAMFCt10pwQxkEyedp0585P2-j6FMPgUfbrOZoppAGlDg3BpSnUvdadH6eUkevNMPhY0NTnNK97ZNA4T1Vx69ElGnOafBhQXa4P7gfabNM0W1-eNo86E4t_djjPmu8fP1xffFpcfb38fHF-tXBcUb6Qtm2NcKI1vrMM244IbAW3gjDrlPG0a6UllLdW8pYyB6YjmHhg1LGOc0vPmnd733G2G986P0zZRD3msDF5q5MJ-s_OEHq9TrcaQBEGvBq8Ohjk9HP2ZdKbUJyP0Qw-zUXLFcZ8RUQF3_wVBIkVSEWE_KcnsGpIJFRQ7EGXUynZd8fBAetd6vo-db1LXd-nXoXPf3_2UXaIufZfHvqmOBO7bAYXyhGTghKsWMXe77G7EP32Py_X11--7QpUURB0N8vrvUkf1v1dyF7vZSW5UL-arpwGvSN_ARR03sw</recordid><startdate>19871201</startdate><enddate>19871201</enddate><creator>Eusebi, F</creator><creator>Grassi, F</creator><creator>Molinaro, M</creator><creator>Zani, B M</creator><general>The Physiological Society</general><general>Blackwell</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19871201</creationdate><title>Acetylcholine regulation of nicotinic receptor channels through a putative G protein in chick myotubes</title><author>Eusebi, F ; Grassi, F ; Molinaro, M ; Zani, B M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5935-7bdda6c6daefb40bf260b65b624bc9ae3fd7b235db75d34c1af202e143c4f55b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>acetylcholine</topic><topic>Acetylcholine - pharmacology</topic><topic>Action Potentials - drug effects</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - pharmacology</topic><topic>Cells, Cultured</topic><topic>Chick Embryo</topic><topic>Cyclic AMP - pharmacology</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>Experimental organogenesis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>guanine nucleotide-binding proteins</topic><topic>Guanosine 5'-O-(3-Thiotriphosphate)</topic><topic>Guanosine Diphosphate - analogs &amp; derivatives</topic><topic>Guanosine Diphosphate - pharmacology</topic><topic>Guanosine Triphosphate - analogs &amp; derivatives</topic><topic>Guanosine Triphosphate - pharmacology</topic><topic>Ion Channels - drug effects</topic><topic>membrane currents</topic><topic>Muscles - embryology</topic><topic>Muscles - physiology</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Organogenesis. Physiological fonctions</topic><topic>Receptors, Nicotinic - physiology</topic><topic>skeletal muscle</topic><topic>Thionucleotides - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eusebi, F</creatorcontrib><creatorcontrib>Grassi, F</creatorcontrib><creatorcontrib>Molinaro, M</creatorcontrib><creatorcontrib>Zani, B M</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>Neurosciences Abstracts</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><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>Eusebi, F</au><au>Grassi, F</au><au>Molinaro, M</au><au>Zani, B M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acetylcholine regulation of nicotinic receptor channels through a putative G protein in chick myotubes</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1987-12-01</date><risdate>1987</risdate><volume>393</volume><issue>1</issue><spage>635</spage><epage>645</epage><pages>635-645</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><coden>JPHYA7</coden><abstract>1. Single-channel currents induced by acetylcholine (ACh) were recorded from unstriated and non-innervated embryonic chick myotubes using the cell-attached patch-clamp technique. 2. ACh applied to the non-patched membrane decreased both channel opening probability and conductance. These ACh-induced effects occurred also when the non-patched membrane was exposed to nominally Ca2+-free extracellular medium, but were absent when it was treated with curare. 3. ACh-induced membrane current recorded under whole-cell patch-clamp conditions decreased in amplitude and time course when myotubes were intracellularly loaded with guanosine-5'-O-(3-thiotriphosphate) GTP gamma S), but not with guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) or cyclic adenosine-5'-monophosphate (cyclic AMP). Internal perfusion of GTP gamma S affected the ACh-induced openings in a similar manner to the non-patch ACh application. 4. These results suggest that ACh, in addition to its direct effect, acts indirectly on the nicotinic receptor channels by delivering an intracellular messenger and through the activation of a putative G protein.</abstract><cop>Oxford</cop><pub>The Physiological Society</pub><pmid>2451747</pmid><doi>10.1113/jphysiol.1987.sp016845</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; IngentaConnect Free/Open Access Journals; Wiley Online Library All Journals; PubMed Central; Alma/SFX Local Collection
subjects acetylcholine
Acetylcholine - pharmacology
Action Potentials - drug effects
Animals
Biological and medical sciences
Calcium - pharmacology
Cells, Cultured
Chick Embryo
Cyclic AMP - pharmacology
Embryology: invertebrates and vertebrates. Teratology
Experimental organogenesis
Fundamental and applied biological sciences. Psychology
guanine nucleotide-binding proteins
Guanosine 5'-O-(3-Thiotriphosphate)
Guanosine Diphosphate - analogs & derivatives
Guanosine Diphosphate - pharmacology
Guanosine Triphosphate - analogs & derivatives
Guanosine Triphosphate - pharmacology
Ion Channels - drug effects
membrane currents
Muscles - embryology
Muscles - physiology
Nerve Tissue Proteins - physiology
Organogenesis. Physiological fonctions
Receptors, Nicotinic - physiology
skeletal muscle
Thionucleotides - pharmacology
title Acetylcholine regulation of nicotinic receptor channels through a putative G protein in chick myotubes
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