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dc.contributor.authorKenemuth, Jessica K.
dc.contributor.authorHennessy, Shane P.
dc.contributor.authorHanson, Ryan J.
dc.contributor.authorHensler, Allison J.
dc.contributor.authorCoates, E. Lee
dc.date.accessioned2014-01-09T15:19:56Z
dc.date.available2014-01-09T15:19:56Z
dc.date.issued2013-11-09
dc.identifier.citationKenemuth, Jessica K., Shane P. Hennessy, Ryan J. Hanson, Allison J. Hensler, and E. Lee Coates. "Investigation of Nasal CO2 Receptor Transduction Mechanisms in Wild-Type and GC-D Knockout Mice." Chemical Senses 38, no. 9 (November 09, 2013): 769-781.en_US
dc.identifier.issn1464-3553
dc.identifier.urihttp://hdl.handle.net/10456/35722
dc.description.abstractThe main olfactory system of mice contains a small subset of olfactory sensory neurons (OSNs) that are stimulated by CO2. The objective of this study was to record olfactory receptor responses to a range of CO2 concentrations to further elucidate steps in the proposed CO2 transduction pathway in mice. Electro-olfactograms (EOGs) were recorded before and after inhibiting specific steps in the CO2 transduction pathway with topically applied inhibitors. Inhibition of extracellular carbonic anhydrase (CA) did not significantly affect EOG responses to CO2 but did decrease EOG responses to several control odorants. Inhibition of intracellular CA or cyclic nucleotide-gated channels attenuated EOG responses to CO2, confirming the role of these components in CO2 sensing in mice. We also show that, like canonical OSNs, CO2-sensitive OSNs depend on Ca2+-activated Cl− channels for depolarization of receptor neurons. Lastly, we found that guanylyl cyclase-D knockout mice were still able to respond to CO2, indicating that other pathways may exist for the detection of low concentrations of nasal CO2. We discuss these findings as they relate to previous studies on CO2-sensitive OSNs in mice and other animals.en_US
dc.description.sponsorshipThis work was supported by the Shanbrom Student and Faculty Research Fund and the Wells Foundation Student-Faculty Research Fund, which are intramural grants provided by Allegheny College’s Dean of the College.en_US
dc.language.isoen_USen_US
dc.publisherOxford University Pressen_US
dc.relation.ispartofChemical Sensesen_US
dc.relation.isversionofhttp://dx.doi.org/10.1093/chemse/bjt044en_US
dc.rightsThis is a pre-copyedited, author-produced PDF of an article accepted for publication in Chemical Senses following peer review. The definitive publisher-authenticated version of Investigation of nasal CO2 receptor transduction mechanisms in wild-type and GC-D knockout mice is available online at: http://dx.doi.org/10.1093/chemse/bjt044en_US
dc.subjectcarbonic anhydraseen_US
dc.subjectcGMPen_US
dc.subjectchloride channelsen_US
dc.subjectCNG channelsen_US
dc.subjectolfactionen_US
dc.subjectolfactory sensory neuronsen_US
dc.titleInvestigation of nasal CO2 receptor transduction mechanisms in wild-type and GC-D knockout miceen_US
dc.typePostprinten_US
dc.contributor.departmentBiologyen_US
dc.contributor.departmentNeuroscienceen_US
dc.description.embargoFinal manuscripts will be available on DSpace after November 9, 2014.en_US
dc.citation.volume38en_US
dc.citation.issue9en_US
dc.citation.spage769en_US
dc.citation.epage781en_US
dc.identifier.doi10.1093/chemse/bjt044


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