Desensitizing Function of Calcium Mobilized by the Postsynaptic Neuronal-Type Nicotinic Acetylcholine Receptors at the Neuromuscular Junction
Neuronal-type nicotinic acetylcholine receptors (N-nAChR) are co-localized with muscle-type (M-)nAChR in the postjunctional endplate membrane of adult skeletal muscle fibers. The postsynaptic desensitizing functions of the N-nAChR at the neuromuscular junction and at single skeletal muscle cells hav...
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Veröffentlicht in: | YAKUGAKU ZASSHI 1999/01/01, Vol.119(1), pp.1-15 |
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description | Neuronal-type nicotinic acetylcholine receptors (N-nAChR) are co-localized with muscle-type (M-)nAChR in the postjunctional endplate membrane of adult skeletal muscle fibers. The postsynaptic desensitizing functions of the N-nAChR at the neuromuscular junction and at single skeletal muscle cells have been investigated using aequorin luminescence and fluorescence confocal imaging. A biphasic elevation of local intracellular Ca2+ is elicited by prolonged nicotinic action at the mouse muscle endplates. The contractile fast and noncontractile slow Ca2+ components are operated by postsynaptic M- and colocalized N-type nAChR, respectively. We have named the latter slow one RAMIC (receptor-activity modulating intracellular Ca2+). The N-nAChR are activated by nicotine and choline, and RAMIC are antagonized by methyllycaconitine and dihydro-β-erythroidine. Neuromuscular functions may be regulated by a dual nAChR system to maintain the normal postsynaptic excitability. Certain N-nAChR may be also endowed with the same functional role in the central nervous system. |
doi_str_mv | 10.1248/yakushi1947.119.1_1 |
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The postsynaptic desensitizing functions of the N-nAChR at the neuromuscular junction and at single skeletal muscle cells have been investigated using aequorin luminescence and fluorescence confocal imaging. A biphasic elevation of local intracellular Ca2+ is elicited by prolonged nicotinic action at the mouse muscle endplates. The contractile fast and noncontractile slow Ca2+ components are operated by postsynaptic M- and colocalized N-type nAChR, respectively. We have named the latter slow one RAMIC (receptor-activity modulating intracellular Ca2+). The N-nAChR are activated by nicotine and choline, and RAMIC are antagonized by methyllycaconitine and dihydro-β-erythroidine. Neuromuscular functions may be regulated by a dual nAChR system to maintain the normal postsynaptic excitability. 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The postsynaptic desensitizing functions of the N-nAChR at the neuromuscular junction and at single skeletal muscle cells have been investigated using aequorin luminescence and fluorescence confocal imaging. A biphasic elevation of local intracellular Ca2+ is elicited by prolonged nicotinic action at the mouse muscle endplates. The contractile fast and noncontractile slow Ca2+ components are operated by postsynaptic M- and colocalized N-type nAChR, respectively. We have named the latter slow one RAMIC (receptor-activity modulating intracellular Ca2+). The N-nAChR are activated by nicotine and choline, and RAMIC are antagonized by methyllycaconitine and dihydro-β-erythroidine. Neuromuscular functions may be regulated by a dual nAChR system to maintain the normal postsynaptic excitability. Certain N-nAChR may be also endowed with the same functional role in the central nervous system.</description><subject>Aconitine - analogs & derivatives</subject><subject>Aconitine - pharmacology</subject><subject>Animals</subject><subject>Calcium - antagonists & inhibitors</subject><subject>Calcium - metabolism</subject><subject>Calcium - physiology</subject><subject>Calcium Signaling - physiology</subject><subject>Choline - pharmacology</subject><subject>desensitization</subject><subject>Excitatory Postsynaptic Potentials</subject><subject>Mice</subject><subject>neuromuscular junction</subject><subject>Neuromuscular Junction - metabolism</subject><subject>Neuromuscular Junction - physiology</subject><subject>neuronal-type nicotinic acetylcholine receptor</subject><subject>Nicotine - pharmacology</subject><subject>noncontractile slow calcium mobilization</subject><subject>receptor-activity modulating intracellular calcium</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Receptors, Nicotinic - physiology</subject><subject>single skeletal muscle cell</subject><issn>0031-6903</issn><issn>1347-5231</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptUctu1DAUtRCojEq_ACF5xW4GO87E8bIaaAsqBaGytpybm47BsYPtLNJ_4J8xndGIBV5cSz4P655DyGvONryq23eL-TmnveWqlhvO1YZr_oysuKjlelsJ_pysGBN83SgmXpKLlGzHWFXOlrdn5EypqpJMrsjv95jQJ5vto_UP9Gr2kG3wNAx0ZxzYeaSfQ2edfcSedgvNe6RfQ8pp8WbKFugdzjF449b3y4T0zkLI1pf3S8C8ONgHZz3Sbwg45RATNfnJ40k2zglmZyL9dPz2FXkxGJfw4nifk-9XH-53N-vbL9cfd5e3a6iZymXBoZEDwACy7gch2x5a1sK24qICo1jbI2s6rloA1UA1tEKyXpimKRlIrlCck7cH3ymGXzOmrEebAJ0zHsOcdKO2skTVFqI4ECGGlCIOeop2NHHRnOm_Peh_etClB116KKo3R_u5G7E_aY6pF_z6gP9I2TzgCTexJOrwf56HeWLA3kSNXvwBw9ejNg</recordid><startdate>19990101</startdate><enddate>19990101</enddate><creator>KIMURA, Ikuko</creator><creator>TSUNEKI, Hiroshi</creator><creator>DEZAKI, Katsuya</creator><creator>NOJIMA, Hiroshi</creator><general>The Pharmaceutical Society of Japan</general><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>7X8</scope></search><sort><creationdate>19990101</creationdate><title>Desensitizing Function of Calcium Mobilized by the Postsynaptic Neuronal-Type Nicotinic Acetylcholine Receptors at the Neuromuscular Junction</title><author>KIMURA, Ikuko ; TSUNEKI, Hiroshi ; DEZAKI, Katsuya ; NOJIMA, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c409t-52f67fccfc74df378dc808c52132ca908de06b198cc96c2f8370d3a66b00719e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>jpn</language><creationdate>1999</creationdate><topic>Aconitine - analogs & derivatives</topic><topic>Aconitine - pharmacology</topic><topic>Animals</topic><topic>Calcium - antagonists & inhibitors</topic><topic>Calcium - metabolism</topic><topic>Calcium - physiology</topic><topic>Calcium Signaling - physiology</topic><topic>Choline - pharmacology</topic><topic>desensitization</topic><topic>Excitatory Postsynaptic Potentials</topic><topic>Mice</topic><topic>neuromuscular junction</topic><topic>Neuromuscular Junction - metabolism</topic><topic>Neuromuscular Junction - physiology</topic><topic>neuronal-type nicotinic acetylcholine receptor</topic><topic>Nicotine - pharmacology</topic><topic>noncontractile slow calcium mobilization</topic><topic>receptor-activity modulating intracellular calcium</topic><topic>Receptors, Nicotinic - metabolism</topic><topic>Receptors, Nicotinic - physiology</topic><topic>single skeletal muscle cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KIMURA, Ikuko</creatorcontrib><creatorcontrib>TSUNEKI, Hiroshi</creatorcontrib><creatorcontrib>DEZAKI, Katsuya</creatorcontrib><creatorcontrib>NOJIMA, Hiroshi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>YAKUGAKU ZASSHI</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KIMURA, Ikuko</au><au>TSUNEKI, Hiroshi</au><au>DEZAKI, Katsuya</au><au>NOJIMA, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Desensitizing Function of Calcium Mobilized by the Postsynaptic Neuronal-Type Nicotinic Acetylcholine Receptors at the Neuromuscular Junction</atitle><jtitle>YAKUGAKU ZASSHI</jtitle><addtitle>YAKUGAKU ZASSHI</addtitle><date>1999-01-01</date><risdate>1999</risdate><volume>119</volume><issue>1</issue><spage>1</spage><epage>15</epage><pages>1-15</pages><issn>0031-6903</issn><eissn>1347-5231</eissn><abstract>Neuronal-type nicotinic acetylcholine receptors (N-nAChR) are co-localized with muscle-type (M-)nAChR in the postjunctional endplate membrane of adult skeletal muscle fibers. The postsynaptic desensitizing functions of the N-nAChR at the neuromuscular junction and at single skeletal muscle cells have been investigated using aequorin luminescence and fluorescence confocal imaging. A biphasic elevation of local intracellular Ca2+ is elicited by prolonged nicotinic action at the mouse muscle endplates. The contractile fast and noncontractile slow Ca2+ components are operated by postsynaptic M- and colocalized N-type nAChR, respectively. We have named the latter slow one RAMIC (receptor-activity modulating intracellular Ca2+). The N-nAChR are activated by nicotine and choline, and RAMIC are antagonized by methyllycaconitine and dihydro-β-erythroidine. Neuromuscular functions may be regulated by a dual nAChR system to maintain the normal postsynaptic excitability. Certain N-nAChR may be also endowed with the same functional role in the central nervous system.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>9922707</pmid><doi>10.1248/yakushi1947.119.1_1</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aconitine - analogs & derivatives Aconitine - pharmacology Animals Calcium - antagonists & inhibitors Calcium - metabolism Calcium - physiology Calcium Signaling - physiology Choline - pharmacology desensitization Excitatory Postsynaptic Potentials Mice neuromuscular junction Neuromuscular Junction - metabolism Neuromuscular Junction - physiology neuronal-type nicotinic acetylcholine receptor Nicotine - pharmacology noncontractile slow calcium mobilization receptor-activity modulating intracellular calcium Receptors, Nicotinic - metabolism Receptors, Nicotinic - physiology single skeletal muscle cell |
title | Desensitizing Function of Calcium Mobilized by the Postsynaptic Neuronal-Type Nicotinic Acetylcholine Receptors at the Neuromuscular Junction |
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