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Intravenous anaesthetics inhibit nicotinic acetylcholine receptor‐mediated currents and Ca2+ transients in rat intracardiac ganglion neurons
1 The effects of intravenous (i.v.) anaesthetics on nicotinic acetylcholine receptor (nAChR)‐induced transients in intracellular free Ca2+ concentration ([Ca2+]i) and membrane currents were investigated in neonatal rat intracardiac neurons. 2 In fura‐2‐loaded neurons, nAChR activation evoked a trans...
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| Published in: | British journal of pharmacology 2005-01, Vol.144 (1), p.98-107 |
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| container_title | British journal of pharmacology |
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| creator | Weber, Martin Motin, Leonid Gaul, Simon Beker, Friederike Fink, Rainer H A Adams, David J |
| description | 1
The effects of intravenous (i.v.) anaesthetics on nicotinic acetylcholine receptor (nAChR)‐induced transients in intracellular free Ca2+ concentration ([Ca2+]i) and membrane currents were investigated in neonatal rat intracardiac neurons.
2
In fura‐2‐loaded neurons, nAChR activation evoked a transient increase in [Ca2+]I, which was inhibited reversibly and selectively by clinically relevant concentrations of thiopental. The half‐maximal concentration for thiopental inhibition of nAChR‐induced [Ca2+]i transients was 28 μM, close to the estimated clinical EC50 (clinically relevant (half‐maximal) effective concentration) of thiopental.
3
In fura‐2‐loaded neurons, voltage clamped at −60 mV to eliminate any contribution of voltage‐gated Ca2+ channels, thiopental (25 μM) simultaneously inhibited nAChR‐induced increases in [Ca2+]i and peak current amplitudes. Thiopental inhibited nAChR‐induced peak current amplitudes in dialysed whole‐cell recordings by ∼ 40% at −120, −80 and −40 mV holding potential, indicating that the inhibition is voltage independent.
4
The barbiturate, pentobarbital and the dissociative anaesthetic, ketamine, used at clinical EC50 were also shown to inhibit nAChR‐induced increases in [Ca2+]i by ∼40%.
5
Thiopental (25 μM) did not inhibit caffeine‐, muscarine‐ or ATP‐evoked increases in [Ca2+]i, indicating that inhibition of Ca2+ release from internal stores via either ryanodine receptor or inositol‐1,4,5‐trisphosphate receptor channels is unlikely.
6
Depolarization‐activated Ca2+ channel currents were unaffected in the presence of thiopental (25 μM), pentobarbital (50 μM) and ketamine (10 μM).
7
In conclusion, i.v. anaesthetics inhibit nAChR‐induced currents and [Ca2+]i transients in intracardiac neurons by binding to nAChRs and thereby may contribute to changes in heart rate and cardiac output under clinical conditions.
British Journal of Pharmacology (2005) 144, 98–107. doi:10.1038/sj.bjp.0705942 |
| doi_str_mv | 10.1038/sj.bjp.0705942 |
| format | article |
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The effects of intravenous (i.v.) anaesthetics on nicotinic acetylcholine receptor (nAChR)‐induced transients in intracellular free Ca2+ concentration ([Ca2+]i) and membrane currents were investigated in neonatal rat intracardiac neurons.
2
In fura‐2‐loaded neurons, nAChR activation evoked a transient increase in [Ca2+]I, which was inhibited reversibly and selectively by clinically relevant concentrations of thiopental. The half‐maximal concentration for thiopental inhibition of nAChR‐induced [Ca2+]i transients was 28 μM, close to the estimated clinical EC50 (clinically relevant (half‐maximal) effective concentration) of thiopental.
3
In fura‐2‐loaded neurons, voltage clamped at −60 mV to eliminate any contribution of voltage‐gated Ca2+ channels, thiopental (25 μM) simultaneously inhibited nAChR‐induced increases in [Ca2+]i and peak current amplitudes. Thiopental inhibited nAChR‐induced peak current amplitudes in dialysed whole‐cell recordings by ∼ 40% at −120, −80 and −40 mV holding potential, indicating that the inhibition is voltage independent.
4
The barbiturate, pentobarbital and the dissociative anaesthetic, ketamine, used at clinical EC50 were also shown to inhibit nAChR‐induced increases in [Ca2+]i by ∼40%.
5
Thiopental (25 μM) did not inhibit caffeine‐, muscarine‐ or ATP‐evoked increases in [Ca2+]i, indicating that inhibition of Ca2+ release from internal stores via either ryanodine receptor or inositol‐1,4,5‐trisphosphate receptor channels is unlikely.
6
Depolarization‐activated Ca2+ channel currents were unaffected in the presence of thiopental (25 μM), pentobarbital (50 μM) and ketamine (10 μM).
7
In conclusion, i.v. anaesthetics inhibit nAChR‐induced currents and [Ca2+]i transients in intracardiac neurons by binding to nAChRs and thereby may contribute to changes in heart rate and cardiac output under clinical conditions.
British Journal of Pharmacology (2005) 144, 98–107. doi:10.1038/sj.bjp.0705942</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0705942</identifier><identifier>PMID: 15644873</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acetylcholine - pharmacology ; Anesthetics, Dissociative - pharmacology ; Anesthetics, Intravenous - pharmacology ; Animals ; Animals, Newborn ; Barbiturates - pharmacology ; Biological and medical sciences ; caffeine ; Calcium - metabolism ; Cells, Cultured ; Electric Conductivity ; Fluorescent Dyes ; Fura-2 ; Ganglia, Parasympathetic - cytology ; Ganglia, Parasympathetic - metabolism ; Ganglia, Parasympathetic - physiology ; ganglionic transmission ; Heart - innervation ; Intracardiac ganglia ; intracellular Ca2 ; intravenous anaesthetics ; ketamine ; Ketamine - pharmacology ; Medical sciences ; Neurons - drug effects ; Neurons - metabolism ; Neurons - physiology ; nicotinic acetylcholine receptor ; Patch-Clamp Techniques ; pentobarbital ; Pentobarbital - pharmacology ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; Receptors, Nicotinic - drug effects ; Receptors, Nicotinic - physiology ; thiopental ; Thiopental - pharmacology</subject><ispartof>British journal of pharmacology, 2005-01, Vol.144 (1), p.98-107</ispartof><rights>2005 British Pharmacological Society</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2005</rights><rights>Copyright 2005, Nature Publishing Group 2005 Nature Publishing Group</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/PMC1575970/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575970/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16480164$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15644873$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weber, Martin</creatorcontrib><creatorcontrib>Motin, Leonid</creatorcontrib><creatorcontrib>Gaul, Simon</creatorcontrib><creatorcontrib>Beker, Friederike</creatorcontrib><creatorcontrib>Fink, Rainer H A</creatorcontrib><creatorcontrib>Adams, David J</creatorcontrib><title>Intravenous anaesthetics inhibit nicotinic acetylcholine receptor‐mediated currents and Ca2+ transients in rat intracardiac ganglion neurons</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1
The effects of intravenous (i.v.) anaesthetics on nicotinic acetylcholine receptor (nAChR)‐induced transients in intracellular free Ca2+ concentration ([Ca2+]i) and membrane currents were investigated in neonatal rat intracardiac neurons.
2
In fura‐2‐loaded neurons, nAChR activation evoked a transient increase in [Ca2+]I, which was inhibited reversibly and selectively by clinically relevant concentrations of thiopental. The half‐maximal concentration for thiopental inhibition of nAChR‐induced [Ca2+]i transients was 28 μM, close to the estimated clinical EC50 (clinically relevant (half‐maximal) effective concentration) of thiopental.
3
In fura‐2‐loaded neurons, voltage clamped at −60 mV to eliminate any contribution of voltage‐gated Ca2+ channels, thiopental (25 μM) simultaneously inhibited nAChR‐induced increases in [Ca2+]i and peak current amplitudes. Thiopental inhibited nAChR‐induced peak current amplitudes in dialysed whole‐cell recordings by ∼ 40% at −120, −80 and −40 mV holding potential, indicating that the inhibition is voltage independent.
4
The barbiturate, pentobarbital and the dissociative anaesthetic, ketamine, used at clinical EC50 were also shown to inhibit nAChR‐induced increases in [Ca2+]i by ∼40%.
5
Thiopental (25 μM) did not inhibit caffeine‐, muscarine‐ or ATP‐evoked increases in [Ca2+]i, indicating that inhibition of Ca2+ release from internal stores via either ryanodine receptor or inositol‐1,4,5‐trisphosphate receptor channels is unlikely.
6
Depolarization‐activated Ca2+ channel currents were unaffected in the presence of thiopental (25 μM), pentobarbital (50 μM) and ketamine (10 μM).
7
In conclusion, i.v. anaesthetics inhibit nAChR‐induced currents and [Ca2+]i transients in intracardiac neurons by binding to nAChRs and thereby may contribute to changes in heart rate and cardiac output under clinical conditions.
British Journal of Pharmacology (2005) 144, 98–107. doi:10.1038/sj.bjp.0705942</description><subject>Acetylcholine - pharmacology</subject><subject>Anesthetics, Dissociative - pharmacology</subject><subject>Anesthetics, Intravenous - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Barbiturates - pharmacology</subject><subject>Biological and medical sciences</subject><subject>caffeine</subject><subject>Calcium - metabolism</subject><subject>Cells, Cultured</subject><subject>Electric Conductivity</subject><subject>Fluorescent Dyes</subject><subject>Fura-2</subject><subject>Ganglia, Parasympathetic - cytology</subject><subject>Ganglia, Parasympathetic - metabolism</subject><subject>Ganglia, Parasympathetic - physiology</subject><subject>ganglionic transmission</subject><subject>Heart - innervation</subject><subject>Intracardiac ganglia</subject><subject>intracellular Ca2</subject><subject>intravenous anaesthetics</subject><subject>ketamine</subject><subject>Ketamine - pharmacology</subject><subject>Medical sciences</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>nicotinic acetylcholine receptor</subject><subject>Patch-Clamp Techniques</subject><subject>pentobarbital</subject><subject>Pentobarbital - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Nicotinic - drug effects</subject><subject>Receptors, Nicotinic - physiology</subject><subject>thiopental</subject><subject>Thiopental - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNpdksuKFDEUhoMoTju6dSlB0I1Um1RuVZsBbdQZGNCFrsOpVLo7RXVSJqmR3s0TDD6jT2LaaR11kwPnfPn5zwWhp5QsKWHN6zQsu2FaEkVEy-t7aEG5kpVgDb2PFoQQVVHaNCfoUUoDIaWoxEN0QoXkvFFsgW4ufI5wZX2YEwYPNuWtzc4k7PzWdS5j70zIrrwYjM370WzD6LzF0Ro75RB_XH_f2d5Btj02c4zW54NSj1dQv8JF3Cf3K-c8jpBLKDkDsXwxeAN-M7rgsbdzDD49Rg_WMCb75BhP0Zf37z6vzqvLjx8uVm8uq4kxISvoiCw9AHTc9qztBDcNoX1t1rytO0mobPs1KNoLapgQQBtje2I6SylnHRfsFJ3d6k5zV9wbezA16im6HcS9DuD0vxXvtnoTrjQVSrSKFIGXR4EYvs5lanrnkrHjCN6WUWqpmBSilQV8_h84hDn60pyuqaItZ6It0LO_7fzx8XtPBXhxBCAZGNdlqsalO07y0r_khWO33Dc32v1dnejDteg06HIt-ngt-u2n81oWjz8BxTC4NQ</recordid><startdate>200501</startdate><enddate>200501</enddate><creator>Weber, Martin</creator><creator>Motin, Leonid</creator><creator>Gaul, Simon</creator><creator>Beker, Friederike</creator><creator>Fink, Rainer H A</creator><creator>Adams, David J</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200501</creationdate><title>Intravenous anaesthetics inhibit nicotinic acetylcholine receptor‐mediated currents and Ca2+ transients in rat intracardiac ganglion neurons</title><author>Weber, Martin ; Motin, Leonid ; Gaul, Simon ; Beker, Friederike ; Fink, Rainer H A ; Adams, David J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p3356-ab06156aab4ed39b54c801d2cf492b60169dfa71d51c355a18ced0cbe1143b453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Anesthetics, Dissociative - pharmacology</topic><topic>Anesthetics, Intravenous - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Barbiturates - pharmacology</topic><topic>Biological and medical sciences</topic><topic>caffeine</topic><topic>Calcium - metabolism</topic><topic>Cells, Cultured</topic><topic>Electric Conductivity</topic><topic>Fluorescent Dyes</topic><topic>Fura-2</topic><topic>Ganglia, Parasympathetic - cytology</topic><topic>Ganglia, Parasympathetic - metabolism</topic><topic>Ganglia, Parasympathetic - physiology</topic><topic>ganglionic transmission</topic><topic>Heart - innervation</topic><topic>Intracardiac ganglia</topic><topic>intracellular Ca2</topic><topic>intravenous anaesthetics</topic><topic>ketamine</topic><topic>Ketamine - pharmacology</topic><topic>Medical sciences</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>nicotinic acetylcholine receptor</topic><topic>Patch-Clamp Techniques</topic><topic>pentobarbital</topic><topic>Pentobarbital - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Nicotinic - drug effects</topic><topic>Receptors, Nicotinic - physiology</topic><topic>thiopental</topic><topic>Thiopental - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weber, Martin</creatorcontrib><creatorcontrib>Motin, Leonid</creatorcontrib><creatorcontrib>Gaul, Simon</creatorcontrib><creatorcontrib>Beker, Friederike</creatorcontrib><creatorcontrib>Fink, Rainer H A</creatorcontrib><creatorcontrib>Adams, David J</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Biological Science Journals</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weber, Martin</au><au>Motin, Leonid</au><au>Gaul, Simon</au><au>Beker, Friederike</au><au>Fink, Rainer H A</au><au>Adams, David J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intravenous anaesthetics inhibit nicotinic acetylcholine receptor‐mediated currents and Ca2+ transients in rat intracardiac ganglion neurons</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2005-01</date><risdate>2005</risdate><volume>144</volume><issue>1</issue><spage>98</spage><epage>107</epage><pages>98-107</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1
The effects of intravenous (i.v.) anaesthetics on nicotinic acetylcholine receptor (nAChR)‐induced transients in intracellular free Ca2+ concentration ([Ca2+]i) and membrane currents were investigated in neonatal rat intracardiac neurons.
2
In fura‐2‐loaded neurons, nAChR activation evoked a transient increase in [Ca2+]I, which was inhibited reversibly and selectively by clinically relevant concentrations of thiopental. The half‐maximal concentration for thiopental inhibition of nAChR‐induced [Ca2+]i transients was 28 μM, close to the estimated clinical EC50 (clinically relevant (half‐maximal) effective concentration) of thiopental.
3
In fura‐2‐loaded neurons, voltage clamped at −60 mV to eliminate any contribution of voltage‐gated Ca2+ channels, thiopental (25 μM) simultaneously inhibited nAChR‐induced increases in [Ca2+]i and peak current amplitudes. Thiopental inhibited nAChR‐induced peak current amplitudes in dialysed whole‐cell recordings by ∼ 40% at −120, −80 and −40 mV holding potential, indicating that the inhibition is voltage independent.
4
The barbiturate, pentobarbital and the dissociative anaesthetic, ketamine, used at clinical EC50 were also shown to inhibit nAChR‐induced increases in [Ca2+]i by ∼40%.
5
Thiopental (25 μM) did not inhibit caffeine‐, muscarine‐ or ATP‐evoked increases in [Ca2+]i, indicating that inhibition of Ca2+ release from internal stores via either ryanodine receptor or inositol‐1,4,5‐trisphosphate receptor channels is unlikely.
6
Depolarization‐activated Ca2+ channel currents were unaffected in the presence of thiopental (25 μM), pentobarbital (50 μM) and ketamine (10 μM).
7
In conclusion, i.v. anaesthetics inhibit nAChR‐induced currents and [Ca2+]i transients in intracardiac neurons by binding to nAChRs and thereby may contribute to changes in heart rate and cardiac output under clinical conditions.
British Journal of Pharmacology (2005) 144, 98–107. doi:10.1038/sj.bjp.0705942</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15644873</pmid><doi>10.1038/sj.bjp.0705942</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British journal of pharmacology, 2005-01, Vol.144 (1), p.98-107 |
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| source | Open Access: PubMed Central; Wiley |
| subjects | Acetylcholine - pharmacology Anesthetics, Dissociative - pharmacology Anesthetics, Intravenous - pharmacology Animals Animals, Newborn Barbiturates - pharmacology Biological and medical sciences caffeine Calcium - metabolism Cells, Cultured Electric Conductivity Fluorescent Dyes Fura-2 Ganglia, Parasympathetic - cytology Ganglia, Parasympathetic - metabolism Ganglia, Parasympathetic - physiology ganglionic transmission Heart - innervation Intracardiac ganglia intracellular Ca2 intravenous anaesthetics ketamine Ketamine - pharmacology Medical sciences Neurons - drug effects Neurons - metabolism Neurons - physiology nicotinic acetylcholine receptor Patch-Clamp Techniques pentobarbital Pentobarbital - pharmacology Pharmacology. Drug treatments Rats Rats, Wistar Receptors, Nicotinic - drug effects Receptors, Nicotinic - physiology thiopental Thiopental - pharmacology |
| title | Intravenous anaesthetics inhibit nicotinic acetylcholine receptor‐mediated currents and Ca2+ transients in rat intracardiac ganglion neurons |
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