ω‐Conotoxin GVIA‐resistant neurotransmitter release from postganglionic sympathetic nerves in the guinea‐pig vas deferens and its modulation by presynaptic receptors
Intracellular recording techniques were used to study neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals in the guinea‐pig isolated vas deferens. Recently, a component of action potential‐evoked release which is insensitive to high concentrations of the selective N‐typ...
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| Veröffentlicht in: | British journal of pharmacology 1998-01, Vol.123 (2), p.167-172 |
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| description | Intracellular recording techniques were used to study neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals in the guinea‐pig isolated vas deferens.
Recently, a component of action potential‐evoked release which is insensitive to high concentrations of the selective N‐type calcium channel blocker ω‐conotoxin GVIA termed ‘residual release’ has been described. Under these conditions, release of the neurotransmitter ATP evoked by trains of low frequency stimuli is abolished, but at higher frequencies a substantial component of release is revealed.
‘Residual release’ was studied with trains of 5 or 10 stimuli at stimulation frequencies of 10, 20 and 50 Hz. The α2‐adrenoceptor agonist clonidine (30–100 nM) inhibited ‘residual release’, the degree of inhibition being most marked at the beginning of a train.
The α2‐adrenoceptor antagonist yohimbine (1 μM) induced a marked increase in ‘residual release’ which was dependent on both the frequency of stimulation and the number of stimuli in a train.
Prostaglandin E2 (30 nM) and neuropeptide Y (100 nM) caused a rapid inhibition of ‘residual release’ at all stimulation frequencies examined.
4‐Aminopyridine (100 μM) induced a powerful potential of ‘residual release’ and could reverse the inhibition of ω‐conotoxin GVIA.
‘Residual release’ was modulated through presynaptic α2‐adrenoceptors suggesting that (i) residual release of ATP is subject to α‐autoinhibition through the co‐release of noradrenaline, (ii) noradrenaline release can be triggered by calcium channels other than the N‐type and (iii) when presynaptic receptors are activated, inhibition of transmitter release can occur by mechanisms other than modulation of calcium‐entry through N‐type calcium channels in postganglionic sympathetic nerves. Prostaglandin E2 and neuropeptide Y also modulated neurotransmitter release.
British Journal of Pharmacology (1998) 123, 167–172; doi:10.1038/sj.bjp.0701577 |
| doi_str_mv | 10.1038/sj.bjp.0701577 |
| format | Article |
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Recently, a component of action potential‐evoked release which is insensitive to high concentrations of the selective N‐type calcium channel blocker ω‐conotoxin GVIA termed ‘residual release’ has been described. Under these conditions, release of the neurotransmitter ATP evoked by trains of low frequency stimuli is abolished, but at higher frequencies a substantial component of release is revealed.
‘Residual release’ was studied with trains of 5 or 10 stimuli at stimulation frequencies of 10, 20 and 50 Hz. The α2‐adrenoceptor agonist clonidine (30–100 nM) inhibited ‘residual release’, the degree of inhibition being most marked at the beginning of a train.
The α2‐adrenoceptor antagonist yohimbine (1 μM) induced a marked increase in ‘residual release’ which was dependent on both the frequency of stimulation and the number of stimuli in a train.
Prostaglandin E2 (30 nM) and neuropeptide Y (100 nM) caused a rapid inhibition of ‘residual release’ at all stimulation frequencies examined.
4‐Aminopyridine (100 μM) induced a powerful potential of ‘residual release’ and could reverse the inhibition of ω‐conotoxin GVIA.
‘Residual release’ was modulated through presynaptic α2‐adrenoceptors suggesting that (i) residual release of ATP is subject to α‐autoinhibition through the co‐release of noradrenaline, (ii) noradrenaline release can be triggered by calcium channels other than the N‐type and (iii) when presynaptic receptors are activated, inhibition of transmitter release can occur by mechanisms other than modulation of calcium‐entry through N‐type calcium channels in postganglionic sympathetic nerves. Prostaglandin E2 and neuropeptide Y also modulated neurotransmitter release.
British Journal of Pharmacology (1998) 123, 167–172; doi:10.1038/sj.bjp.0701577</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0701577</identifier><identifier>PMID: 9489603</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>4-Aminopyridine - pharmacology ; Adrenergic alpha-Agonists - pharmacology ; Adrenergic alpha-Antagonists - pharmacology ; Animals ; autoinhibition ; Biological and medical sciences ; Calcium Channel Blockers - pharmacology ; Clonidine - pharmacology ; co‐transmission ; Dinoprostone - pharmacology ; Fundamental and applied biological sciences. Psychology ; Guinea Pigs ; In Vitro Techniques ; Male ; Mice ; Neuropeptide Y - pharmacology ; Neurotransmitter Agents - secretion ; Neurotransmitter release ; N‐type calcium channels ; omega-Conotoxin GVIA ; Peptides - pharmacology ; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ ; Receptors, Adrenergic, alpha-2 - drug effects ; Receptors, Adrenergic, alpha-2 - physiology ; Sympathetic Fibers, Postganglionic - drug effects ; Sympathetic Fibers, Postganglionic - secretion ; sympathetic nerves ; Vas Deferens - innervation ; Vertebrates: nervous system and sense organs ; Yohimbine - pharmacology</subject><ispartof>British journal of pharmacology, 1998-01, Vol.123 (2), p.167-172</ispartof><rights>1998 British Pharmacological Society</rights><rights>1998 INIST-CNRS</rights><rights>Copyright 1998, Nature Publishing Group 1998 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4894-9732b5df250758220dff2c2e781977477a2239e21a4e430443463a290ff9cb483</citedby><cites>FETCH-LOGICAL-c4894-9732b5df250758220dff2c2e781977477a2239e21a4e430443463a290ff9cb483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1565148/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1565148/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2126784$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9489603$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Smith, Amanda B</creatorcontrib><creatorcontrib>Cunnane, Tom C</creatorcontrib><title>ω‐Conotoxin GVIA‐resistant neurotransmitter release from postganglionic sympathetic nerves in the guinea‐pig vas deferens and its modulation by presynaptic receptors</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Intracellular recording techniques were used to study neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals in the guinea‐pig isolated vas deferens.
Recently, a component of action potential‐evoked release which is insensitive to high concentrations of the selective N‐type calcium channel blocker ω‐conotoxin GVIA termed ‘residual release’ has been described. Under these conditions, release of the neurotransmitter ATP evoked by trains of low frequency stimuli is abolished, but at higher frequencies a substantial component of release is revealed.
‘Residual release’ was studied with trains of 5 or 10 stimuli at stimulation frequencies of 10, 20 and 50 Hz. The α2‐adrenoceptor agonist clonidine (30–100 nM) inhibited ‘residual release’, the degree of inhibition being most marked at the beginning of a train.
The α2‐adrenoceptor antagonist yohimbine (1 μM) induced a marked increase in ‘residual release’ which was dependent on both the frequency of stimulation and the number of stimuli in a train.
Prostaglandin E2 (30 nM) and neuropeptide Y (100 nM) caused a rapid inhibition of ‘residual release’ at all stimulation frequencies examined.
4‐Aminopyridine (100 μM) induced a powerful potential of ‘residual release’ and could reverse the inhibition of ω‐conotoxin GVIA.
‘Residual release’ was modulated through presynaptic α2‐adrenoceptors suggesting that (i) residual release of ATP is subject to α‐autoinhibition through the co‐release of noradrenaline, (ii) noradrenaline release can be triggered by calcium channels other than the N‐type and (iii) when presynaptic receptors are activated, inhibition of transmitter release can occur by mechanisms other than modulation of calcium‐entry through N‐type calcium channels in postganglionic sympathetic nerves. Prostaglandin E2 and neuropeptide Y also modulated neurotransmitter release.
British Journal of Pharmacology (1998) 123, 167–172; doi:10.1038/sj.bjp.0701577</description><subject>4-Aminopyridine - pharmacology</subject><subject>Adrenergic alpha-Agonists - pharmacology</subject><subject>Adrenergic alpha-Antagonists - pharmacology</subject><subject>Animals</subject><subject>autoinhibition</subject><subject>Biological and medical sciences</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Clonidine - pharmacology</subject><subject>co‐transmission</subject><subject>Dinoprostone - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guinea Pigs</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Mice</subject><subject>Neuropeptide Y - pharmacology</subject><subject>Neurotransmitter Agents - secretion</subject><subject>Neurotransmitter release</subject><subject>N‐type calcium channels</subject><subject>omega-Conotoxin GVIA</subject><subject>Peptides - pharmacology</subject><subject>Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ</subject><subject>Receptors, Adrenergic, alpha-2 - drug effects</subject><subject>Receptors, Adrenergic, alpha-2 - physiology</subject><subject>Sympathetic Fibers, Postganglionic - drug effects</subject><subject>Sympathetic Fibers, Postganglionic - secretion</subject><subject>sympathetic nerves</subject><subject>Vas Deferens - innervation</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Yohimbine - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxiMEKkvhyg3JB8RtF_9LnFyQ2hW0lSrBAbhaTjLZepXYweMs7K3X3ngQ3oV34Elw2WgFJ0625vv8m_F8Wfac0RWjonyN21W9HVdUUZYr9SBbMKmKZS5K9jBbUErVkrGyfJw9QdxSmkSVn2QnlSyrgopF9uPn3a_b72vvfPTfrCMXn6_OUiEAWozGReJgCj4G43CwMUIgAXowCKQLfiCjx7gxbtNb72xDcD-MJt5ATHcHYQdIEjMVyGayDkwij3ZDdgZJCx0EcEiMa4mNSAbfTr2JCUTqPRnTBHtnxntSgAbG6AM-zR51pkd4Np-n2ad3bz-uL5fX7y-u1mfXyyZ9Sy4rJXidtx3PqcpLzmnbdbzhoEpWKZU2YDgXFXBmJEhBpRSyEIZXtOuqppalOM3eHLjjVA_QNuDSAno9BjuYsNfeWP2v4uyN3vidZnmRsz-AVzMg-C8TYNSDxQb63jjwE2pWSCWo4Mm4Ohib4BEDdMcmjOr7fDVudcpXz_mmBy_-Hu1onwNN-stZN9iYvkvBNRaPNs54oUqZbOJg-2p72P-nqT7_cJmrXIrfPZ_ICA</recordid><startdate>199801</startdate><enddate>199801</enddate><creator>Smith, Amanda B</creator><creator>Cunnane, Tom C</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>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>199801</creationdate><title>ω‐Conotoxin GVIA‐resistant neurotransmitter release from postganglionic sympathetic nerves in the guinea‐pig vas deferens and its modulation by presynaptic receptors</title><author>Smith, Amanda B ; Cunnane, Tom C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4894-9732b5df250758220dff2c2e781977477a2239e21a4e430443463a290ff9cb483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>Adrenergic alpha-Agonists - pharmacology</topic><topic>Adrenergic alpha-Antagonists - pharmacology</topic><topic>Animals</topic><topic>autoinhibition</topic><topic>Biological and medical sciences</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Clonidine - pharmacology</topic><topic>co‐transmission</topic><topic>Dinoprostone - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guinea Pigs</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Mice</topic><topic>Neuropeptide Y - pharmacology</topic><topic>Neurotransmitter Agents - secretion</topic><topic>Neurotransmitter release</topic><topic>N‐type calcium channels</topic><topic>omega-Conotoxin GVIA</topic><topic>Peptides - pharmacology</topic><topic>Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ</topic><topic>Receptors, Adrenergic, alpha-2 - drug effects</topic><topic>Receptors, Adrenergic, alpha-2 - physiology</topic><topic>Sympathetic Fibers, Postganglionic - drug effects</topic><topic>Sympathetic Fibers, Postganglionic - secretion</topic><topic>sympathetic nerves</topic><topic>Vas Deferens - innervation</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>Yohimbine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Smith, Amanda B</creatorcontrib><creatorcontrib>Cunnane, Tom C</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>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>Smith, Amanda B</au><au>Cunnane, Tom C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ω‐Conotoxin GVIA‐resistant neurotransmitter release from postganglionic sympathetic nerves in the guinea‐pig vas deferens and its modulation by presynaptic receptors</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1998-01</date><risdate>1998</risdate><volume>123</volume><issue>2</issue><spage>167</spage><epage>172</epage><pages>167-172</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Intracellular recording techniques were used to study neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals in the guinea‐pig isolated vas deferens.
Recently, a component of action potential‐evoked release which is insensitive to high concentrations of the selective N‐type calcium channel blocker ω‐conotoxin GVIA termed ‘residual release’ has been described. Under these conditions, release of the neurotransmitter ATP evoked by trains of low frequency stimuli is abolished, but at higher frequencies a substantial component of release is revealed.
‘Residual release’ was studied with trains of 5 or 10 stimuli at stimulation frequencies of 10, 20 and 50 Hz. The α2‐adrenoceptor agonist clonidine (30–100 nM) inhibited ‘residual release’, the degree of inhibition being most marked at the beginning of a train.
The α2‐adrenoceptor antagonist yohimbine (1 μM) induced a marked increase in ‘residual release’ which was dependent on both the frequency of stimulation and the number of stimuli in a train.
Prostaglandin E2 (30 nM) and neuropeptide Y (100 nM) caused a rapid inhibition of ‘residual release’ at all stimulation frequencies examined.
4‐Aminopyridine (100 μM) induced a powerful potential of ‘residual release’ and could reverse the inhibition of ω‐conotoxin GVIA.
‘Residual release’ was modulated through presynaptic α2‐adrenoceptors suggesting that (i) residual release of ATP is subject to α‐autoinhibition through the co‐release of noradrenaline, (ii) noradrenaline release can be triggered by calcium channels other than the N‐type and (iii) when presynaptic receptors are activated, inhibition of transmitter release can occur by mechanisms other than modulation of calcium‐entry through N‐type calcium channels in postganglionic sympathetic nerves. Prostaglandin E2 and neuropeptide Y also modulated neurotransmitter release.
British Journal of Pharmacology (1998) 123, 167–172; doi:10.1038/sj.bjp.0701577</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9489603</pmid><doi>10.1038/sj.bjp.0701577</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 4-Aminopyridine - pharmacology Adrenergic alpha-Agonists - pharmacology Adrenergic alpha-Antagonists - pharmacology Animals autoinhibition Biological and medical sciences Calcium Channel Blockers - pharmacology Clonidine - pharmacology co‐transmission Dinoprostone - pharmacology Fundamental and applied biological sciences. Psychology Guinea Pigs In Vitro Techniques Male Mice Neuropeptide Y - pharmacology Neurotransmitter Agents - secretion Neurotransmitter release N‐type calcium channels omega-Conotoxin GVIA Peptides - pharmacology Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ Receptors, Adrenergic, alpha-2 - drug effects Receptors, Adrenergic, alpha-2 - physiology Sympathetic Fibers, Postganglionic - drug effects Sympathetic Fibers, Postganglionic - secretion sympathetic nerves Vas Deferens - innervation Vertebrates: nervous system and sense organs Yohimbine - pharmacology |
| title | ω‐Conotoxin GVIA‐resistant neurotransmitter release from postganglionic sympathetic nerves in the guinea‐pig vas deferens and its modulation by presynaptic receptors |
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