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dc.contributor.authorLiu, Liwang
dc.contributor.authorRittenhouse, Ann R.
dc.date2022-08-11T08:09:34.000
dc.date.accessioned2022-08-23T16:35:44Z
dc.date.available2022-08-23T16:35:44Z
dc.date.issued2000-06-02
dc.date.submitted2009-03-26
dc.identifier.citation<p>J Physiol. 2000 Jun 1;525 Pt 2:391-404.</p>
dc.identifier.issn0022-3751 (Print)
dc.identifier.pmid10835042
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38629
dc.description.abstractWe have characterized the actions of arachidonic acid (AA) on whole cell and unitary calcium (Ca2+) currents in rat neonatal superior cervical ganglion (SCG) neurons using barium (Ba2+) as the charge carrier. Whole cell currents were elicited by stepping the membrane potential from -90 mV to +10 mV. Arachidonic acid (5 microM) was introduced into the bath in the continued presence of 1 microM (+)-202-791, an L-type Ca2+ channel agonist. Under these conditions, the peak current, comprised mainly of N-type current, and a slow, (+)-202-791-induced component of the tail current were inhibited by 67 +/- 6 and 60 +/- 10 %, respectively, indicating that AA inhibits both N- and L-type currents. At a test potential of +30 mV, AA (5 microM) decreased unitary L- and N-type Ca2+ channel open probability (Po) in cell-attached patches that contained a single channel. For both channels, the underlying causes of the decrease in Po were similar. Arachidonic acid caused an increase in the percentage of null sweeps and in the number of null sweeps that clustered together. In sweeps with activity, the average number of openings per sweep decreased, while first latency and mean closed time increased. Arachidonic acid had no significant effect on unitary current amplitude or mean open time. Our findings are the first description of the inhibition of unitary L- and N-type Ca2+ channel activity by AA and are consistent with both channels spending more time in their null mode and with increased dwell time in one or more closed states.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10835042&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2269949/
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectArachidonic Acid
dc.subjectBarium
dc.subjectCalcium
dc.subjectCalcium Channel Blockers
dc.subjectCalcium Channels, L-Type
dc.subjectCalcium Channels, N-Type
dc.subjectIon Transport
dc.subjectKinetics
dc.subjectMembrane Potentials
dc.subjectNeurons
dc.subjectPatch-Clamp Techniques
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectSuperior Cervical Ganglion
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleEffects of arachidonic acid on unitary calcium currents in rat sympathetic neurons
dc.typeJournal Article
dc.source.journaltitleThe Journal of physiology
dc.source.volume525 Pt 2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1490
dc.identifier.contextkey798465
html.description.abstract<p>We have characterized the actions of arachidonic acid (AA) on whole cell and unitary calcium (Ca2+) currents in rat neonatal superior cervical ganglion (SCG) neurons using barium (Ba2+) as the charge carrier. Whole cell currents were elicited by stepping the membrane potential from -90 mV to +10 mV. Arachidonic acid (5 microM) was introduced into the bath in the continued presence of 1 microM (+)-202-791, an L-type Ca2+ channel agonist. Under these conditions, the peak current, comprised mainly of N-type current, and a slow, (+)-202-791-induced component of the tail current were inhibited by 67 +/- 6 and 60 +/- 10 %, respectively, indicating that AA inhibits both N- and L-type currents. At a test potential of +30 mV, AA (5 microM) decreased unitary L- and N-type Ca2+ channel open probability (Po) in cell-attached patches that contained a single channel. For both channels, the underlying causes of the decrease in Po were similar. Arachidonic acid caused an increase in the percentage of null sweeps and in the number of null sweeps that clustered together. In sweeps with activity, the average number of openings per sweep decreased, while first latency and mean closed time increased. Arachidonic acid had no significant effect on unitary current amplitude or mean open time. Our findings are the first description of the inhibition of unitary L- and N-type Ca2+ channel activity by AA and are consistent with both channels spending more time in their null mode and with increased dwell time in one or more closed states.</p>
dc.identifier.submissionpathoapubs/1490
dc.contributor.departmentProgram in Neuroscience
dc.contributor.departmentDepartment of Physiology
dc.source.pages391-404


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