Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons

Abstract The calcium-activated chloride channel anoctamin-2 (Ano2) is thought to amplify transduction currents in olfactory receptor neurons (ORNs), a hypothesis supported by previous studies in dissociated neurons from Ano2 −/− mice. Paradoxically, despite a reduction in transduction currents in An...

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Autores principales:	Joseph D. Zak, Julien Grimaud, Rong-Chang Li, Chih-Chun Lin, Venkatesh N. Murthy
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3aec2c696f2b468d9d6f10a8e92a9143
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spelling	oai:doaj.org-article:3aec2c696f2b468d9d6f10a8e92a91432021-12-02T15:07:52ZCalcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons10.1038/s41598-018-28855-32045-2322https://doaj.org/article/3aec2c696f2b468d9d6f10a8e92a91432018-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-28855-3https://doaj.org/toc/2045-2322Abstract The calcium-activated chloride channel anoctamin-2 (Ano2) is thought to amplify transduction currents in olfactory receptor neurons (ORNs), a hypothesis supported by previous studies in dissociated neurons from Ano2 −/− mice. Paradoxically, despite a reduction in transduction currents in Ano2 −/− ORNs, their spike output for odor stimuli may be higher. We examined the role of Ano2 in ORNs in their native environment in freely breathing mice by imaging activity in ORN axons as they arrive in the olfactory bulb glomeruli. Odor-evoked responses in ORN axons of Ano2 −/− animals were consistently larger for a variety of odorants and concentrations. In an open arena, Ano2 −/− animals took longer to approach a localized odor source than Ano2 +/+ animals, revealing clear olfactory behavioral deficits. Our studies provide the first in vivo evidence toward an alternative or additional role for Ano2 in the olfactory transduction cascade, where it may serve as a feedback mechanism to clamp ORN spike output.Joseph D. ZakJulien GrimaudRong-Chang LiChih-Chun LinVenkatesh N. MurthyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-13 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Joseph D. Zak Julien Grimaud Rong-Chang Li Chih-Chun Lin Venkatesh N. Murthy Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons
description	Abstract The calcium-activated chloride channel anoctamin-2 (Ano2) is thought to amplify transduction currents in olfactory receptor neurons (ORNs), a hypothesis supported by previous studies in dissociated neurons from Ano2 −/− mice. Paradoxically, despite a reduction in transduction currents in Ano2 −/− ORNs, their spike output for odor stimuli may be higher. We examined the role of Ano2 in ORNs in their native environment in freely breathing mice by imaging activity in ORN axons as they arrive in the olfactory bulb glomeruli. Odor-evoked responses in ORN axons of Ano2 −/− animals were consistently larger for a variety of odorants and concentrations. In an open arena, Ano2 −/− animals took longer to approach a localized odor source than Ano2 +/+ animals, revealing clear olfactory behavioral deficits. Our studies provide the first in vivo evidence toward an alternative or additional role for Ano2 in the olfactory transduction cascade, where it may serve as a feedback mechanism to clamp ORN spike output.
format	article
author	Joseph D. Zak Julien Grimaud Rong-Chang Li Chih-Chun Lin Venkatesh N. Murthy
author_facet	Joseph D. Zak Julien Grimaud Rong-Chang Li Chih-Chun Lin Venkatesh N. Murthy
author_sort	Joseph D. Zak
title	Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons
title_short	Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons
title_full	Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons
title_fullStr	Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons
title_full_unstemmed	Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons
title_sort	calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/3aec2c696f2b468d9d6f10a8e92a9143
work_keys_str_mv	AT josephdzak calciumactivatedchloridechannelsclampodorevokedspikeactivityinolfactoryreceptorneurons AT juliengrimaud calciumactivatedchloridechannelsclampodorevokedspikeactivityinolfactoryreceptorneurons AT rongchangli calciumactivatedchloridechannelsclampodorevokedspikeactivityinolfactoryreceptorneurons AT chihchunlin calciumactivatedchloridechannelsclampodorevokedspikeactivityinolfactoryreceptorneurons AT venkateshnmurthy calciumactivatedchloridechannelsclampodorevokedspikeactivityinolfactoryreceptorneurons
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Calcium-activated chloride channels clamp odor-evoked spike activity in olfactory receptor neurons

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