Effects of Ca2+ and K+ channel blockers on nerve impulses recorded from guinea-pig postganglionic sympathetic nerve terminals
1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve impulse recorded from sympathetic nerve terminals innervating the guinea-pig vas deferens in vitro. 2. Perfusing the electrode with Cd2+ (0.1-0.5 mM) had little effect on the con...
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| Veröffentlicht in: | The Journal of physiology 1995-12, Vol.489 (Pt 2), p.389-402 |
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| description | 1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve
impulse recorded from sympathetic nerve terminals innervating the guinea-pig vas deferens in vitro. 2. Perfusing the electrode
with Cd2+ (0.1-0.5 mM) had little effect on the configuration of the nerve impulse. 3. Perfusing the electrode with Ba2+ (1-3
mM) caused the appearance of a second negative-going component of the nerve impulse. Local application of Cd2+ (0.1 mM) had
little affect on this component of the nerve impulse. 4. Perfusing the electrode with 4-aminopyridine (4-AP) and/or tetraethylammonium
(TEA) caused the appearance of a second negative-going component of the nerve impulse. This component has been termed the
late negative-going component (LNC). 5. The LNC produced by local application of 1 mM 4-AP and 10 mM TEA was not changed when
the solution perfusing the electrode contained no added Ca2+, 10 mM Ca2+ or omega-conotoxin GVIA (0.1 microM). Perfusion of
the electrode with Cd2+ (0.1 mM) reduced the amplitude and slowed the time course of the LNC. 6. The LNC was markedly inhibited
when the organ bath was perfused with TEA (10 mM) or 4-AP and TEA (1 and 10 mM, respectively). In some experiments the LNC
was completely abolished. 7. The LNC was reduced in amplitude and slowed in time course when the solution perfusing the organ
bath contained no added Ca2+. A similar effect on the LNC was observed when the solution perfusing the organ bath contained
omega-conotoxin GVIA (0.1 microM), charybdotoxin (0.05 microM) or low concentrations of TEA (0.3-1 mM) or Ba2+ (10-500 microM).
8. Bath application of the alpha 2-adrenoceptor agonist clonidine (0.1-0.3 microM) did not detectably change the LNC. 9. The
results demonstrate that the LNC produced by the local application of K+ blockers is due primarily to K+ efflux from sites
outside the recording electrode and that a part of the change in conductance that underlies this component is due to opening
of Ca(2+)-activated K+ channels. The failure to detect an effect of clonidine on the LNC suggests that activation of presynaptic
alpha 2-adrenoceptors does not change either the K+ or the Ca2+ conductance of the nerve terminals. |
| doi_str_mv | 10.1113/jphysiol.1995.sp021060 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1156767</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1709174096</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5369-b345cac9bf80352374d3c3f384664dc030d85e4184c4cfea3ab655bf01a7fa8f3</originalsourceid><addsrcrecordid>eNqNkc1u1DAUhS0EKtOBRwB5hRBVBjt24mSDBKPyW4kuytpynOvEJbGDnbTKou9ORplWsEGsruVz7icfH4ReUrKjlLK310M7R-u7HS3LbBcHklKSk0doQ3leJkKU7DHaEJKmCRMZfYpOY7wmhDJSlifopCi4yFm2QXfnxoAeI_YG71V6hpWr8bczrFvlHHS46rz-CWHRHXYQbgDbfpi6CBEH0D7UUGMTfI-byTpQyWAbPPg4Nso1nfXOahznflBjC-NyXhEjhN461cVn6IlZBjw_zi368fH8av85ufj-6cv-_UWiM7akqRjPtNJlZQrCspQJXjPNDCt4nvNaE0bqIgNOC665NqCYqvIsqwyhShhVGLZF71buMFU91BrcGFQnh2B7FWbplZV_K862svE3ktIsF7lYAK-OgOB_TRBH2duooeuUAz9FKUQhGF0-fYte_9NIBSmp4KTMF2u-WnXwMQYwD--hRB46lvcdy0PH8r7jZfHFn2ke1o6lLvqHVb-1Hcz_SZVXXy8PF7woU1YcgrxZIa1t2lsbQK5r0WsL4ywXn7wcZSoP5t-5-8zU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1709174096</pqid></control><display><type>article</type><title>Effects of Ca2+ and K+ channel blockers on nerve impulses recorded from guinea-pig postganglionic sympathetic nerve terminals</title><source>MEDLINE</source><source>IngentaConnect Free/Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Brock, J A ; Cunnane, T C</creator><creatorcontrib>Brock, J A ; Cunnane, T C</creatorcontrib><description>1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve
impulse recorded from sympathetic nerve terminals innervating the guinea-pig vas deferens in vitro. 2. Perfusing the electrode
with Cd2+ (0.1-0.5 mM) had little effect on the configuration of the nerve impulse. 3. Perfusing the electrode with Ba2+ (1-3
mM) caused the appearance of a second negative-going component of the nerve impulse. Local application of Cd2+ (0.1 mM) had
little affect on this component of the nerve impulse. 4. Perfusing the electrode with 4-aminopyridine (4-AP) and/or tetraethylammonium
(TEA) caused the appearance of a second negative-going component of the nerve impulse. This component has been termed the
late negative-going component (LNC). 5. The LNC produced by local application of 1 mM 4-AP and 10 mM TEA was not changed when
the solution perfusing the electrode contained no added Ca2+, 10 mM Ca2+ or omega-conotoxin GVIA (0.1 microM). Perfusion of
the electrode with Cd2+ (0.1 mM) reduced the amplitude and slowed the time course of the LNC. 6. The LNC was markedly inhibited
when the organ bath was perfused with TEA (10 mM) or 4-AP and TEA (1 and 10 mM, respectively). In some experiments the LNC
was completely abolished. 7. The LNC was reduced in amplitude and slowed in time course when the solution perfusing the organ
bath contained no added Ca2+. A similar effect on the LNC was observed when the solution perfusing the organ bath contained
omega-conotoxin GVIA (0.1 microM), charybdotoxin (0.05 microM) or low concentrations of TEA (0.3-1 mM) or Ba2+ (10-500 microM).
8. Bath application of the alpha 2-adrenoceptor agonist clonidine (0.1-0.3 microM) did not detectably change the LNC. 9. The
results demonstrate that the LNC produced by the local application of K+ blockers is due primarily to K+ efflux from sites
outside the recording electrode and that a part of the change in conductance that underlies this component is due to opening
of Ca(2+)-activated K+ channels. The failure to detect an effect of clonidine on the LNC suggests that activation of presynaptic
alpha 2-adrenoceptors does not change either the K+ or the Ca2+ conductance of the nerve terminals.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1995.sp021060</identifier><identifier>PMID: 8847635</identifier><language>eng</language><publisher>England: The Physiological Society</publisher><subject>4-Aminopyridine - pharmacology ; Animals ; Barium - pharmacology ; Cadmium - pharmacology ; Calcium - pharmacology ; Calcium Channel Blockers - pharmacology ; Guinea Pigs ; Male ; Membrane Potentials - drug effects ; Potassium Channel Blockers ; Sympathetic Nervous System - drug effects ; Tetraethylammonium ; Tetraethylammonium Compounds - pharmacology</subject><ispartof>The Journal of physiology, 1995-12, Vol.489 (Pt 2), p.389-402</ispartof><rights>1995 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5369-b345cac9bf80352374d3c3f384664dc030d85e4184c4cfea3ab655bf01a7fa8f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1156767/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1156767/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,27901,27902,45550,45551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8847635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brock, J A</creatorcontrib><creatorcontrib>Cunnane, T C</creatorcontrib><title>Effects of Ca2+ and K+ channel blockers on nerve impulses recorded from guinea-pig postganglionic sympathetic nerve terminals</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve
impulse recorded from sympathetic nerve terminals innervating the guinea-pig vas deferens in vitro. 2. Perfusing the electrode
with Cd2+ (0.1-0.5 mM) had little effect on the configuration of the nerve impulse. 3. Perfusing the electrode with Ba2+ (1-3
mM) caused the appearance of a second negative-going component of the nerve impulse. Local application of Cd2+ (0.1 mM) had
little affect on this component of the nerve impulse. 4. Perfusing the electrode with 4-aminopyridine (4-AP) and/or tetraethylammonium
(TEA) caused the appearance of a second negative-going component of the nerve impulse. This component has been termed the
late negative-going component (LNC). 5. The LNC produced by local application of 1 mM 4-AP and 10 mM TEA was not changed when
the solution perfusing the electrode contained no added Ca2+, 10 mM Ca2+ or omega-conotoxin GVIA (0.1 microM). Perfusion of
the electrode with Cd2+ (0.1 mM) reduced the amplitude and slowed the time course of the LNC. 6. The LNC was markedly inhibited
when the organ bath was perfused with TEA (10 mM) or 4-AP and TEA (1 and 10 mM, respectively). In some experiments the LNC
was completely abolished. 7. The LNC was reduced in amplitude and slowed in time course when the solution perfusing the organ
bath contained no added Ca2+. A similar effect on the LNC was observed when the solution perfusing the organ bath contained
omega-conotoxin GVIA (0.1 microM), charybdotoxin (0.05 microM) or low concentrations of TEA (0.3-1 mM) or Ba2+ (10-500 microM).
8. Bath application of the alpha 2-adrenoceptor agonist clonidine (0.1-0.3 microM) did not detectably change the LNC. 9. The
results demonstrate that the LNC produced by the local application of K+ blockers is due primarily to K+ efflux from sites
outside the recording electrode and that a part of the change in conductance that underlies this component is due to opening
of Ca(2+)-activated K+ channels. The failure to detect an effect of clonidine on the LNC suggests that activation of presynaptic
alpha 2-adrenoceptors does not change either the K+ or the Ca2+ conductance of the nerve terminals.</description><subject>4-Aminopyridine - pharmacology</subject><subject>Animals</subject><subject>Barium - pharmacology</subject><subject>Cadmium - pharmacology</subject><subject>Calcium - pharmacology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Guinea Pigs</subject><subject>Male</subject><subject>Membrane Potentials - drug effects</subject><subject>Potassium Channel Blockers</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Tetraethylammonium</subject><subject>Tetraethylammonium Compounds - pharmacology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EKtOBRwB5hRBVBjt24mSDBKPyW4kuytpynOvEJbGDnbTKou9ORplWsEGsruVz7icfH4ReUrKjlLK310M7R-u7HS3LbBcHklKSk0doQ3leJkKU7DHaEJKmCRMZfYpOY7wmhDJSlifopCi4yFm2QXfnxoAeI_YG71V6hpWr8bczrFvlHHS46rz-CWHRHXYQbgDbfpi6CBEH0D7UUGMTfI-byTpQyWAbPPg4Nso1nfXOahznflBjC-NyXhEjhN461cVn6IlZBjw_zi368fH8av85ufj-6cv-_UWiM7akqRjPtNJlZQrCspQJXjPNDCt4nvNaE0bqIgNOC665NqCYqvIsqwyhShhVGLZF71buMFU91BrcGFQnh2B7FWbplZV_K862svE3ktIsF7lYAK-OgOB_TRBH2duooeuUAz9FKUQhGF0-fYte_9NIBSmp4KTMF2u-WnXwMQYwD--hRB46lvcdy0PH8r7jZfHFn2ke1o6lLvqHVb-1Hcz_SZVXXy8PF7woU1YcgrxZIa1t2lsbQK5r0WsL4ywXn7wcZSoP5t-5-8zU</recordid><startdate>19951201</startdate><enddate>19951201</enddate><creator>Brock, J A</creator><creator>Cunnane, T C</creator><general>The Physiological Society</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>7QP</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19951201</creationdate><title>Effects of Ca2+ and K+ channel blockers on nerve impulses recorded from guinea-pig postganglionic sympathetic nerve terminals</title><author>Brock, J A ; Cunnane, T C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5369-b345cac9bf80352374d3c3f384664dc030d85e4184c4cfea3ab655bf01a7fa8f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>4-Aminopyridine - pharmacology</topic><topic>Animals</topic><topic>Barium - pharmacology</topic><topic>Cadmium - pharmacology</topic><topic>Calcium - pharmacology</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Guinea Pigs</topic><topic>Male</topic><topic>Membrane Potentials - drug effects</topic><topic>Potassium Channel Blockers</topic><topic>Sympathetic Nervous System - drug effects</topic><topic>Tetraethylammonium</topic><topic>Tetraethylammonium Compounds - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brock, J A</creatorcontrib><creatorcontrib>Cunnane, T C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences 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>Brock, J A</au><au>Cunnane, T C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Ca2+ and K+ channel blockers on nerve impulses recorded from guinea-pig postganglionic sympathetic nerve terminals</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1995-12-01</date><risdate>1995</risdate><volume>489</volume><issue>Pt 2</issue><spage>389</spage><epage>402</epage><pages>389-402</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve
impulse recorded from sympathetic nerve terminals innervating the guinea-pig vas deferens in vitro. 2. Perfusing the electrode
with Cd2+ (0.1-0.5 mM) had little effect on the configuration of the nerve impulse. 3. Perfusing the electrode with Ba2+ (1-3
mM) caused the appearance of a second negative-going component of the nerve impulse. Local application of Cd2+ (0.1 mM) had
little affect on this component of the nerve impulse. 4. Perfusing the electrode with 4-aminopyridine (4-AP) and/or tetraethylammonium
(TEA) caused the appearance of a second negative-going component of the nerve impulse. This component has been termed the
late negative-going component (LNC). 5. The LNC produced by local application of 1 mM 4-AP and 10 mM TEA was not changed when
the solution perfusing the electrode contained no added Ca2+, 10 mM Ca2+ or omega-conotoxin GVIA (0.1 microM). Perfusion of
the electrode with Cd2+ (0.1 mM) reduced the amplitude and slowed the time course of the LNC. 6. The LNC was markedly inhibited
when the organ bath was perfused with TEA (10 mM) or 4-AP and TEA (1 and 10 mM, respectively). In some experiments the LNC
was completely abolished. 7. The LNC was reduced in amplitude and slowed in time course when the solution perfusing the organ
bath contained no added Ca2+. A similar effect on the LNC was observed when the solution perfusing the organ bath contained
omega-conotoxin GVIA (0.1 microM), charybdotoxin (0.05 microM) or low concentrations of TEA (0.3-1 mM) or Ba2+ (10-500 microM).
8. Bath application of the alpha 2-adrenoceptor agonist clonidine (0.1-0.3 microM) did not detectably change the LNC. 9. The
results demonstrate that the LNC produced by the local application of K+ blockers is due primarily to K+ efflux from sites
outside the recording electrode and that a part of the change in conductance that underlies this component is due to opening
of Ca(2+)-activated K+ channels. The failure to detect an effect of clonidine on the LNC suggests that activation of presynaptic
alpha 2-adrenoceptors does not change either the K+ or the Ca2+ conductance of the nerve terminals.</abstract><cop>England</cop><pub>The Physiological Society</pub><pmid>8847635</pmid><doi>10.1113/jphysiol.1995.sp021060</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 1995-12, Vol.489 (Pt 2), p.389-402 |
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| source | MEDLINE; IngentaConnect Free/Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | 4-Aminopyridine - pharmacology Animals Barium - pharmacology Cadmium - pharmacology Calcium - pharmacology Calcium Channel Blockers - pharmacology Guinea Pigs Male Membrane Potentials - drug effects Potassium Channel Blockers Sympathetic Nervous System - drug effects Tetraethylammonium Tetraethylammonium Compounds - pharmacology |
| title | Effects of Ca2+ and K+ channel blockers on nerve impulses recorded from guinea-pig postganglionic sympathetic nerve terminals |
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