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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Guanosine 3',5'-cyclic monophosphate regulates calcium channels in neurones of rabbit vesical pelvic ganglia.</title><author><name sortKey="Nishimura, T" sort="Nishimura, T" uniqKey="Nishimura T" first="T" last="Nishimura">T. Nishimura</name></author><author><name sortKey="Akasu, T" sort="Akasu, T" uniqKey="Akasu T" first="T" last="Akasu">T. Akasu</name></author><author><name sortKey="Krier, J" sort="Krier, J" uniqKey="Krier J" first="J" last="Krier">J. Krier</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">1338464</idno><idno type="pmc">1175747</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1175747</idno><idno type="RBID">PMC:1175747</idno><date when="1992">1992</date><idno type="wicri:Area/Pmc/Corpus">000200</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000200</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Guanosine 3',5'-cyclic monophosphate regulates calcium channels in neurones of rabbit vesical pelvic ganglia.</title><author><name sortKey="Nishimura, T" sort="Nishimura, T" uniqKey="Nishimura T" first="T" last="Nishimura">T. Nishimura</name></author><author><name sortKey="Akasu, T" sort="Akasu, T" uniqKey="Akasu T" first="T" last="Akasu">T. Akasu</name></author><author><name sortKey="Krier, J" sort="Krier, J" uniqKey="Krier J" first="J" last="Krier">J. Krier</name></author></analytic><series><title level="j">The Journal of Physiology</title><idno type="ISSN">0022-3751</idno><idno type="eISSN">1469-7793</idno><imprint><date when="1992">1992</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>1. The effects of dibutyryl guanosine 3',5'-cyclic monophosphate (db-cyclic GMP) were studied in vitro on calcium channels of neurones in rabbit vesical parasympathetic ganglia, using intracellular and single-electrode voltage-clamp recordings. 2. Db-cyclic GMP (100 microM) caused membrane depolarization associated with a decrease in membrane input resistance and an after-hyperpolarization associated with an increase in membrane input resistance. 3. Db-cyclic GMP (0.01-1 mM) caused a concentration-dependent, transient inward current followed by a long-lasting outward current. Membrane conductance was increased and decreased during the inward and outward currents, respectively. 4. The db-cyclic GMP-induced inward current was depressed in nominally calcium-free solutions, by cobalt (1 mM) and nicardipine (10 microM). The mean reversal potentials of the inward current were +42 and -20 mV in the presence and absence of calcium in the external solution, respectively. 5. The db-cyclic GMP-induced inward current was not altered by lowering the external sodium concentration, raising external potassium concentration or by intracellular injection of caesium. 6. A calcium-insensitive component of the db-cyclic GMP-induced current was increased by lowering the external chloride concentration and blocked by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid, a chloride channel blocker. 7. Voltage-dependent, high-threshold calcium currents were depressed during the db-cyclic GMP-induced inward current and facilitated during the outward current. 8. Cyclic GMP was less potent than db-cyclic GMP in causing both inward and outward currents or modulation of calcium currents. GTP, GDP, GMP, guanosine, 8-bromoadenosine 3',5'-cyclic monophosphate and forskolin did not alter the holding current or voltage-dependent calcium currents. 9. It is concluded that intracellular cyclic GMP causes not only activation of resting calcium and chloride channels but also a transient depression followed by long-lasting facilitation of voltage-dependent calcium currents in neurones of vesical parasympathetic ganglia.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><label>Fig. 1</label><graphic xlink:href="jphysiol00425-0557-a" xlink:role="562"></graphic></fig></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Physiol</journal-id><journal-title>The Journal of Physiology</journal-title><issn pub-type="ppub">0022-3751</issn><issn pub-type="epub">1469-7793</issn></journal-meta><article-meta><article-id pub-id-type="pmid">1338464</article-id><article-id pub-id-type="pmc">1175747</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Guanosine 3',5'-cyclic monophosphate regulates calcium channels in neurones of rabbit vesical pelvic ganglia.</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Nishimura</surname><given-names>T</given-names></name></contrib><contrib contrib-type="author"><name><surname>Akasu</surname><given-names>T</given-names></name></contrib><contrib contrib-type="author"><name><surname>Krier</surname><given-names>J</given-names></name></contrib></contrib-group><aff>Department of Physiology, Kurume University School of Medicine, Japan.</aff><pub-date pub-type="ppub"><month>11</month><year>1992</year></pub-date><volume>457</volume><fpage>559</fpage><lpage>574</lpage><abstract><p>1. The effects of dibutyryl guanosine 3',5'-cyclic monophosphate (db-cyclic GMP) were studied in vitro on calcium channels of neurones in rabbit vesical parasympathetic ganglia, using intracellular and single-electrode voltage-clamp recordings. 2. Db-cyclic GMP (100 microM) caused membrane depolarization associated with a decrease in membrane input resistance and an after-hyperpolarization associated with an increase in membrane input resistance. 3. Db-cyclic GMP (0.01-1 mM) caused a concentration-dependent, transient inward current followed by a long-lasting outward current. Membrane conductance was increased and decreased during the inward and outward currents, respectively. 4. The db-cyclic GMP-induced inward current was depressed in nominally calcium-free solutions, by cobalt (1 mM) and nicardipine (10 microM). The mean reversal potentials of the inward current were +42 and -20 mV in the presence and absence of calcium in the external solution, respectively. 5. The db-cyclic GMP-induced inward current was not altered by lowering the external sodium concentration, raising external potassium concentration or by intracellular injection of caesium. 6. A calcium-insensitive component of the db-cyclic GMP-induced current was increased by lowering the external chloride concentration and blocked by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid, a chloride channel blocker. 7. Voltage-dependent, high-threshold calcium currents were depressed during the db-cyclic GMP-induced inward current and facilitated during the outward current. 8. Cyclic GMP was less potent than db-cyclic GMP in causing both inward and outward currents or modulation of calcium currents. GTP, GDP, GMP, guanosine, 8-bromoadenosine 3',5'-cyclic monophosphate and forskolin did not alter the holding current or voltage-dependent calcium currents. 9. It is concluded that intracellular cyclic GMP causes not only activation of resting calcium and chloride channels but also a transient depression followed by long-lasting facilitation of voltage-dependent calcium currents in neurones of vesical parasympathetic ganglia.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><label>Fig. 1</label><graphic xlink:href="jphysiol00425-0557-a" xlink:role="562"></graphic></fig></sec></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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