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dc.contributor.authorFrenz, Christopher T.en_US
dc.contributor.authorHansen, Anneen_US
dc.contributor.authorDupuis, Nicholas D.en_US
dc.contributor.authorShultz, Nicoleen_US
dc.contributor.authorLevinson, Simon R.en_US
dc.contributor.authorFinger, Thomas E.en_US
dc.contributor.authorDionne, Vincent E.en_US
dc.date.accessioned2018-08-20T18:46:32Z
dc.date.available2018-08-20T18:46:32Z
dc.date.issued2014-09-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000341687200008&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=6e74115fe3da270499c3d65c9b17d654
dc.identifier.citationChristopher T Frenz, Anne Hansen, Nicholas D Dupuis, Nicole Shultz, Simon R Levinson, Thomas E Finger, Vincent E Dionne. 2014. "Na(V)1.5 sodium channel window currents contribute to spontaneous firing in olfactory sensory neurons." Journal Of Neurophysiology, Volume 112, Issue 5, pp. 1091 - 1104 (14). https://doi.org/10.1152/jn.00154.2014
dc.identifier.issn0022-3077
dc.identifier.issn1522-1598
dc.identifier.urihttps://hdl.handle.net/2144/30822
dc.description.abstractOlfactory sensory neurons (OSNs) fire spontaneously as well as in response to odor; both forms of firing are physiologically important. We studied voltage-gated Na+ channels in OSNs to assess their role in spontaneous activity. Whole cell patch-clamp recordings from OSNs demonstrated both tetrodotoxin-sensitive and tetrodotoxin-resistant components of Na+ current. RT-PCR showed mRNAs for five of the nine different Na+ channel α-subunits in olfactory tissue; only one was tetrodotoxin resistant, the so-called cardiac subtype NaV1.5. Immunohistochemical analysis indicated that NaV1.5 is present in the apical knob of OSN dendrites but not in the axon. The NaV1.5 channels in OSNs exhibited two important features: 1) a half-inactivation potential near −100 mV, well below the resting potential, and 2) a window current centered near the resting potential. The negative half-inactivation potential renders most NaV1.5 channels in OSNs inactivated at the resting potential, while the window current indicates that the minor fraction of noninactivated NaV1.5 channels have a small probability of opening spontaneously at the resting potential. When the tetrodotoxin-sensitive Na+ channels were blocked by nanomolar tetrodotoxin at the resting potential, spontaneous firing was suppressed as expected. Furthermore, selectively blocking NaV1.5 channels with Zn2+ in the absence of tetrodotoxin also suppressed spontaneous firing, indicating that NaV1.5 channels are required for spontaneous activity despite resting inactivation. We propose that window currents produced by noninactivated NaV1.5 channels are one source of the generator potentials that trigger spontaneous firing, while the upstroke and propagation of action potentials in OSNs are borne by the tetrodotoxin-sensitive Na+ channel subtypes.en_US
dc.description.sponsorshipThis work was aided by support from Boston University, the Rocky Mountain Taste and Smell Center Core for Cellular Visualization and Analysis [National Institute on Deafness and Other Communication Disorders (NIDCD) P30 DC-04657; D. Restrepo, principal investigator], and NIDCD Grants DC-04863 to V. Dionne and DC-006070 to D. Restrepo and T. E. Finger. (Boston University; P30 DC-04657 - Rocky Mountain Taste and Smell Center Core for Cellular Visualization and Analysis [National Institute on Deafness and Other Communication Disorders (NIDCD)]; DC-04863 - Rocky Mountain Taste and Smell Center Core for Cellular Visualization and Analysis [National Institute on Deafness and Other Communication Disorders (NIDCD)]; DC-006070 - Rocky Mountain Taste and Smell Center Core for Cellular Visualization and Analysis [National Institute on Deafness and Other Communication Disorders (NIDCD)])en_US
dc.description.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4122723/
dc.format.extentp. 1091 - 1104en_US
dc.languageEnglish
dc.publisherAMER PHYSIOLOGICAL SOCen_US
dc.relation.ispartofJournal Of Neurophysiology
dc.relation.isversionofhttps://doi.org/10.1152/jn.00154.2014
dc.rightsCopyright © 2014 the American Physiological Societyen_US
dc.subjectScience & technologyen_US
dc.subjectLife sciences & biomedicineen_US
dc.subjectNeurosciencesen_US
dc.subjectPhysiologyen_US
dc.subjectNeurosciences & neurologyen_US
dc.subjectNa(V)1.5 sodium channelsen_US
dc.subjectWindow currentsen_US
dc.subjectSpontaneous firingen_US
dc.subjectOlfactory sensory neuronsen_US
dc.subjectOlfactionen_US
dc.subjectMouseen_US
dc.subjectCellsen_US
dc.subjectNaV1.5 sodium channelsen_US
dc.subjectAction potentialsen_US
dc.subjectAnimalsen_US
dc.subjectFemaleen_US
dc.subjectMaleen_US
dc.subjectMiceen_US
dc.subjectMice, inbred C57BLen_US
dc.subjectNAV1.5 voltage-gated sodium channelen_US
dc.subjectOlfactory mucosaen_US
dc.subjectSensory receptor xellsen_US
dc.subjectMedical and health sciencesen_US
dc.subjectPsychology and cognitive sciencesen_US
dc.titleNa(V)1.5 sodium channel window currents contribute to spontaneous firing in olfactory sensory neuronsen_US
dc.typeArticleen_US
dc.description.versionAccepted manuscripten_US
pubs.elements-sourceweb-of-scienceen_US
pubs.notesEmbargo: No embargoen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Arts & Sciencesen_US
pubs.organisational-groupBoston University, College of Arts & Sciences, Department of Biologyen_US
pubs.publication-statusPublisheden_US


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