{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/21576"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/21576","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"The cyclic AMP-activated sodium current in the molluscan neuron: A kinetic analysis of regulation by diffusion, phosphodiesterase and calcium ion","abstract":"Effects of cyclic AMP on pedal neurons of the marine mollusc, Pleurobranchaea californica were studied by intracellular iontophoresis of cyclic AMP under voltage clamp condition. The I$\\sb{\\rm Na,cAMP}$ response to cyclic AMP injection is resistant to protein kinase inhibitors, and is very likely mediated by direct cyclic AMP binding to the channel receptor. The slow I$\\sb{\\rm Na,cAMP}$ is regulated by diffusion-hydrolysis kinetics: it varied in latency to current onset, latency to peak amplitude, and amplitude with the distance of the membrane to the tip of the iontophoretic cyclic AMP injection electrode; the phosphodiesterase inhibitor isobutylmethyxanthine (IBMX) in increasing concentrations motonically decreased the decay rates of the I$\\sb{\\rm Na,cAMP}$ response. A diffusion-reaction model incorporating terms for diffusion and degradation of cyclic AMP accurately fitted the time course of I$\\sb{\\rm Na,cAMP}$ response to a pulse of cyclic AMP. An application of the model allows extraction of phosphodiesterase activity as a first-order rate constant from the exponential decay phase of the I$\\sb{\\rm Na,cAMP}$ response.","abstract_html":"Effects of cyclic AMP on pedal neurons of the marine mollusc, Pleurobranchaea californica were studied by intracellular iontophoresis of cyclic AMP under voltage clamp condition. The I$\\sb{\\rm Na,cAMP}$ response to cyclic AMP injection is resistant to protein kinase inhibitors, and is very likely mediated by direct cyclic AMP binding to the channel receptor. The slow I$\\sb{\\rm Na,cAMP}$ is regulated by diffusion-hydrolysis kinetics: it varied in latency to current onset, latency to peak amplitude, and amplitude with the distance of the membrane to the tip of the iontophoretic cyclic AMP injection electrode; the phosphodiesterase inhibitor isobutylmethyxanthine (IBMX) in increasing concentrations motonically decreased the decay rates of the I$\\sb{\\rm Na,cAMP}$ response. A diffusion-reaction model incorporating terms for diffusion and degradation of cyclic AMP accurately fitted the time course of I$\\sb{\\rm Na,cAMP}$ response to a pulse of cyclic AMP. An application of the model allows extraction of phosphodiesterase activity as a first-order rate constant from the exponential decay phase of the I$\\sb{\\rm Na,cAMP}$ response.","abstract_has_math":true,"creators":["Huang, Rong-Chi"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Physiology","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T13:12:44Z","date_published":"2011-05-07T13:12:44Z","updated_at":"2026-07-22T22:25:18Z","subjects":["Biology, Neuroscience","Biology, Animal Physiology"],"languages":["eng"],"rights":["Copyright 1989 Huang, Rong-Chi"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9010897","(UMI)AAI9010897"],"render_values":[{"text":"AAI9010897","href":null,"code":true},{"text":"(UMI)AAI9010897","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/21576","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Huang, Rong-Chi"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-05-07T13:12:44Z","10000-01-01","1989"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Physiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Neuroscience","Biology, Animal Physiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 1989 Huang, Rong-Chi"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9010897","(UMI)AAI9010897","http://hdl.handle.net/2142/21576"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Effects of cyclic AMP on pedal neurons of the marine mollusc, Pleurobranchaea californica were studied by intracellular iontophoresis of cyclic AMP under voltage clamp condition. The I$\\sb{\\rm Na,cAMP}$ response to cyclic AMP injection is resistant to protein kinase inhibitors, and is very likely mediated by direct cyclic AMP binding to the channel receptor. The slow I$\\sb{\\rm Na,cAMP}$ is regulated by diffusion-hydrolysis kinetics: it varied in latency to current onset, latency to peak amplitude, and amplitude with the distance of the membrane to the tip of the iontophoretic cyclic AMP injection electrode; the phosphodiesterase inhibitor isobutylmethyxanthine (IBMX) in increasing concentrations motonically decreased the decay rates of the I$\\sb{\\rm Na,cAMP}$ response. A diffusion-reaction model incorporating terms for diffusion and degradation of cyclic AMP accurately fitted the time course of I$\\sb{\\rm Na,cAMP}$ response to a pulse of cyclic AMP. An application of the model allows extraction of phosphodiesterase activity as a first-order rate constant from the exponential decay phase of the I$\\sb{\\rm Na,cAMP}$ response.","Intracellular Ca$\\sp{2+}$ suppresses the I$\\sb{\\rm Na,cAMP}$ response; in contrast, serotonin, IBMX, and tonic injection of cyclic AMP tonically activate the I$\\sb{\\rm Na,cAMP}$ response and reduce its sensitivity to Ca$\\sp{2+}$ modulation. The mutually antagonistic effects of intracellular Ca$\\sp{2+}$ and cyclic AMP on the I$\\sb{\\rm Na,cAMP}$ response were best explained in terms of a competitive binding model: intracellular Ca$\\sp{2+}$ suppresses I$\\sb{\\rm Na,cAMP}$ by decreasing the channel binding for cyclic AMP, and cyclic AMP decreases the channel affinity for intracellular Ca$\\sp{2+}$. The competitive binding model also predicts supporting results of experiment tests.","Extracellular Ca$\\sp{2+}$ also regulates I$\\sb{\\rm Na,cAMP}$ by affecting cyclic AMP binding affinity in addition to its effect on channel conductance. Low extracellular Ca$\\sp{2+}$ converts a low maximum amplitude/high cyclic AMP binding affinity current to a high maximum amplitude/low cyclic AMP binding affinity one; this design augments the intracellular Ca$\\sp{2+}$ suppressive effect and thus serves as a safeguard preventing high cyclic AMP-induced pathological excitation. In conclusion, low extracellular Ca$\\sp{2+}$ complements intracellular Ca$\\sp{2+}$ in regulating I$\\sb{\\rm Na,cAMP}$ response.","Made available in DSpace on 2011-05-07T13:12:44Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9010897.pdf: 6089267 bytes, checksum: c2f5cd2ca325d22d2a0f4fc8ec78ce2a (MD5) Previous issue date: 1989","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:51:43Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:23:46-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"]},{"key":"dc:title","label":"Title","values":["The cyclic AMP-activated sodium current in the molluscan neuron: A kinetic analysis of regulation by diffusion, phosphodiesterase and calcium ion"]}]}],"canonical_facts":{"dc:creator":["Huang, Rong-Chi"],"dc:date":["2011-05-07T13:12:44Z","10000-01-01","1989"],"dc:description":["Effects of cyclic AMP on pedal neurons of the marine mollusc, Pleurobranchaea californica were studied by intracellular iontophoresis of cyclic AMP under voltage clamp condition. The I$\\sb{\\rm Na,cAMP}$ response to cyclic AMP injection is resistant to protein kinase inhibitors, and is very likely mediated by direct cyclic AMP binding to the channel receptor. The slow I$\\sb{\\rm Na,cAMP}$ is regulated by diffusion-hydrolysis kinetics: it varied in latency to current onset, latency to peak amplitude, and amplitude with the distance of the membrane to the tip of the iontophoretic cyclic AMP injection electrode; the phosphodiesterase inhibitor isobutylmethyxanthine (IBMX) in increasing concentrations motonically decreased the decay rates of the I$\\sb{\\rm Na,cAMP}$ response. A diffusion-reaction model incorporating terms for diffusion and degradation of cyclic AMP accurately fitted the time course of I$\\sb{\\rm Na,cAMP}$ response to a pulse of cyclic AMP. An application of the model allows extraction of phosphodiesterase activity as a first-order rate constant from the exponential decay phase of the I$\\sb{\\rm Na,cAMP}$ response.","Intracellular Ca$\\sp{2+}$ suppresses the I$\\sb{\\rm Na,cAMP}$ response; in contrast, serotonin, IBMX, and tonic injection of cyclic AMP tonically activate the I$\\sb{\\rm Na,cAMP}$ response and reduce its sensitivity to Ca$\\sp{2+}$ modulation. The mutually antagonistic effects of intracellular Ca$\\sp{2+}$ and cyclic AMP on the I$\\sb{\\rm Na,cAMP}$ response were best explained in terms of a competitive binding model: intracellular Ca$\\sp{2+}$ suppresses I$\\sb{\\rm Na,cAMP}$ by decreasing the channel binding for cyclic AMP, and cyclic AMP decreases the channel affinity for intracellular Ca$\\sp{2+}$. The competitive binding model also predicts supporting results of experiment tests.","Extracellular Ca$\\sp{2+}$ also regulates I$\\sb{\\rm Na,cAMP}$ by affecting cyclic AMP binding affinity in addition to its effect on channel conductance. Low extracellular Ca$\\sp{2+}$ converts a low maximum amplitude/high cyclic AMP binding affinity current to a high maximum amplitude/low cyclic AMP binding affinity one; this design augments the intracellular Ca$\\sp{2+}$ suppressive effect and thus serves as a safeguard preventing high cyclic AMP-induced pathological excitation. In conclusion, low extracellular Ca$\\sp{2+}$ complements intracellular Ca$\\sp{2+}$ in regulating I$\\sb{\\rm Na,cAMP}$ response.","Made available in DSpace on 2011-05-07T13:12:44Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9010897.pdf: 6089267 bytes, checksum: c2f5cd2ca325d22d2a0f4fc8ec78ce2a (MD5) Previous issue date: 1989","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:51:43Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:23:46-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"],"dc:identifier":["AAI9010897","(UMI)AAI9010897","http://hdl.handle.net/2142/21576"],"dc:language":["eng"],"dc:rights":["Copyright 1989 Huang, Rong-Chi"],"dc:subject":["Biology, Neuroscience","Biology, Animal Physiology"],"dc:title":["The cyclic AMP-activated sodium current in the molluscan neuron: A kinetic analysis of regulation by diffusion, phosphodiesterase and calcium ion"],"dc:type":["text"],"thesis:degree_discipline":["Physiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:18Z"}