Neuronal Chloride Accumulation in Olfactory Epithelium of Mice Lacking NKCC1
Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati, Cincinnati, Ohio Submitted 12 September 2005; accepted in final form 28 November 2005 When stimulated with odorants, olfactory receptor neurons (ORNs) produce a depolarizing receptor current. In isolated ORNs, much of t...
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container_issue | 3 |
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container_title | Journal of neurophysiology |
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creator | Nickell, William T Kleene, Nancy K Gesteland, Robert C Kleene, Steven J |
description | Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati, Cincinnati, Ohio
Submitted 12 September 2005;
accepted in final form 28 November 2005
When stimulated with odorants, olfactory receptor neurons (ORNs) produce a depolarizing receptor current. In isolated ORNs, much of this current is caused by an efflux of Cl . This implies that the neurons have one or more mechanisms for accumulating cytoplasmic Cl at rest. Whether odors activate an efflux of Cl in intact olfactory epithelium, where the ionic environment is poorly characterized, has not been previously determined. In mouse olfactory epithelium, we found that >80% of the summated electrical response to odors is blocked by niflumic acid or flufenamic acid, each of which inhibits Ca 2+ -activated Cl channels in ORNs. This indicates that ORNs accumulate Cl in situ. Recent evidence has shown that NKCC1, a Na + -K + -2Cl cotransporter, contributes to Cl accumulation in mammalian ORNs. However, we find that the epithelial response to odors is only reduced by 39% in mice carrying a null mutation in Nkcc1 . As in the wild-type, most of the response is blocked by niflumic acid or flufenamic acid, indicating that the underlying current is carried by Cl . We conclude that ORNs effectively accumulate Cl in situ even in the absence of NKCC1. The Cl -transport mechanism underlying this accumulation has not yet been identified.
Address for reprint requests and other correspondence: S. J. Kleene, Dept. of Cell Biology, Neurobiology, and Anatomy, Univ. of Cincinnati, PO Box 670667, Cincinnati, OH 45267-0667 (E-mail: steve{at}syrano.acb.uc.edu ) |
doi_str_mv | 10.1152/jn.00962.2005 |
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Submitted 12 September 2005;
accepted in final form 28 November 2005
When stimulated with odorants, olfactory receptor neurons (ORNs) produce a depolarizing receptor current. In isolated ORNs, much of this current is caused by an efflux of Cl . This implies that the neurons have one or more mechanisms for accumulating cytoplasmic Cl at rest. Whether odors activate an efflux of Cl in intact olfactory epithelium, where the ionic environment is poorly characterized, has not been previously determined. In mouse olfactory epithelium, we found that >80% of the summated electrical response to odors is blocked by niflumic acid or flufenamic acid, each of which inhibits Ca 2+ -activated Cl channels in ORNs. This indicates that ORNs accumulate Cl in situ. Recent evidence has shown that NKCC1, a Na + -K + -2Cl cotransporter, contributes to Cl accumulation in mammalian ORNs. However, we find that the epithelial response to odors is only reduced by 39% in mice carrying a null mutation in Nkcc1 . As in the wild-type, most of the response is blocked by niflumic acid or flufenamic acid, indicating that the underlying current is carried by Cl . We conclude that ORNs effectively accumulate Cl in situ even in the absence of NKCC1. The Cl -transport mechanism underlying this accumulation has not yet been identified.
Address for reprint requests and other correspondence: S. J. Kleene, Dept. of Cell Biology, Neurobiology, and Anatomy, Univ. of Cincinnati, PO Box 670667, Cincinnati, OH 45267-0667 (E-mail: steve{at}syrano.acb.uc.edu )</description><identifier>ISSN: 0022-3077</identifier><identifier>EISSN: 1522-1598</identifier><identifier>DOI: 10.1152/jn.00962.2005</identifier><identifier>PMID: 16319203</identifier><language>eng</language><publisher>United States: Am Phys Soc</publisher><subject>Animals ; Chlorine - metabolism ; Membrane Potentials - physiology ; Mice ; Olfactory Mucosa - physiology ; Olfactory Receptor Neurons - physiology ; Sodium-Potassium-Chloride Symporters - deficiency ; Solute Carrier Family 12, Member 2</subject><ispartof>Journal of neurophysiology, 2006-03, Vol.95 (3), p.2003-2006</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-8522f6ac00e68a6635c1b135111f30fd6798ec029459b41f37f792cd26b7e6a3</citedby><cites>FETCH-LOGICAL-c558t-8522f6ac00e68a6635c1b135111f30fd6798ec029459b41f37f792cd26b7e6a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16319203$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nickell, William T</creatorcontrib><creatorcontrib>Kleene, Nancy K</creatorcontrib><creatorcontrib>Gesteland, Robert C</creatorcontrib><creatorcontrib>Kleene, Steven J</creatorcontrib><title>Neuronal Chloride Accumulation in Olfactory Epithelium of Mice Lacking NKCC1</title><title>Journal of neurophysiology</title><addtitle>J Neurophysiol</addtitle><description>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati, Cincinnati, Ohio
Submitted 12 September 2005;
accepted in final form 28 November 2005
When stimulated with odorants, olfactory receptor neurons (ORNs) produce a depolarizing receptor current. In isolated ORNs, much of this current is caused by an efflux of Cl . This implies that the neurons have one or more mechanisms for accumulating cytoplasmic Cl at rest. Whether odors activate an efflux of Cl in intact olfactory epithelium, where the ionic environment is poorly characterized, has not been previously determined. In mouse olfactory epithelium, we found that >80% of the summated electrical response to odors is blocked by niflumic acid or flufenamic acid, each of which inhibits Ca 2+ -activated Cl channels in ORNs. This indicates that ORNs accumulate Cl in situ. Recent evidence has shown that NKCC1, a Na + -K + -2Cl cotransporter, contributes to Cl accumulation in mammalian ORNs. However, we find that the epithelial response to odors is only reduced by 39% in mice carrying a null mutation in Nkcc1 . As in the wild-type, most of the response is blocked by niflumic acid or flufenamic acid, indicating that the underlying current is carried by Cl . We conclude that ORNs effectively accumulate Cl in situ even in the absence of NKCC1. The Cl -transport mechanism underlying this accumulation has not yet been identified.
Address for reprint requests and other correspondence: S. J. Kleene, Dept. of Cell Biology, Neurobiology, and Anatomy, Univ. of Cincinnati, PO Box 670667, Cincinnati, OH 45267-0667 (E-mail: steve{at}syrano.acb.uc.edu )</description><subject>Animals</subject><subject>Chlorine - metabolism</subject><subject>Membrane Potentials - physiology</subject><subject>Mice</subject><subject>Olfactory Mucosa - physiology</subject><subject>Olfactory Receptor Neurons - physiology</subject><subject>Sodium-Potassium-Chloride Symporters - deficiency</subject><subject>Solute Carrier Family 12, Member 2</subject><issn>0022-3077</issn><issn>1522-1598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFv0zAYhi0EYmVw5Ip8glO6z_ZsxxekKdoA0W2X3i3XcRoXJw5OMui_x6XVYIedbH1-vsevXoTeE1gSwunFrl8CKEGXFIC_QIs8owXhqnyJFgD5zkDKM_RmHHcAIDnQ1-iMCEYUBbZAqzs3p9ibgKs2xORrh6-snbs5mMnHHvse34fG2CmmPb4e_NS64OcOxwbfeuvwytgfvt_iu-9VRd6iV40Jo3t3Os_R-uZ6XX0tVvdfvlVXq8JyXk5FmSM2wlgAJ0ojBOOWbAjjhJCGQVMLqUpngapLrjaXeSYbqaitqdhIJww7R5-P2mHedK62rp-SCXpIvjNpr6Px-ulL71u9jQ-aMKmEoFnw8SRI8efsxkl3frQuBNO7OI-aSCilUDKDxRG0KY5jcs3jJwT0oX696_Xf-vWh_sx_-D_ZP_rUdwbYEWj9tv3lk9NDux99DHG71zdzCGv3e8pSxTU7KJke6iZvfXp-Kyd4pNkfWOuggA</recordid><startdate>20060301</startdate><enddate>20060301</enddate><creator>Nickell, William T</creator><creator>Kleene, Nancy K</creator><creator>Gesteland, Robert C</creator><creator>Kleene, Steven J</creator><general>Am Phys Soc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20060301</creationdate><title>Neuronal Chloride Accumulation in Olfactory Epithelium of Mice Lacking NKCC1</title><author>Nickell, William T ; Kleene, Nancy K ; Gesteland, Robert C ; Kleene, Steven J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-8522f6ac00e68a6635c1b135111f30fd6798ec029459b41f37f792cd26b7e6a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Chlorine - metabolism</topic><topic>Membrane Potentials - physiology</topic><topic>Mice</topic><topic>Olfactory Mucosa - physiology</topic><topic>Olfactory Receptor Neurons - physiology</topic><topic>Sodium-Potassium-Chloride Symporters - deficiency</topic><topic>Solute Carrier Family 12, Member 2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nickell, William T</creatorcontrib><creatorcontrib>Kleene, Nancy K</creatorcontrib><creatorcontrib>Gesteland, Robert C</creatorcontrib><creatorcontrib>Kleene, Steven J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neurophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nickell, William T</au><au>Kleene, Nancy K</au><au>Gesteland, Robert C</au><au>Kleene, Steven J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuronal Chloride Accumulation in Olfactory Epithelium of Mice Lacking NKCC1</atitle><jtitle>Journal of neurophysiology</jtitle><addtitle>J Neurophysiol</addtitle><date>2006-03-01</date><risdate>2006</risdate><volume>95</volume><issue>3</issue><spage>2003</spage><epage>2006</epage><pages>2003-2006</pages><issn>0022-3077</issn><eissn>1522-1598</eissn><abstract>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati, Cincinnati, Ohio
Submitted 12 September 2005;
accepted in final form 28 November 2005
When stimulated with odorants, olfactory receptor neurons (ORNs) produce a depolarizing receptor current. In isolated ORNs, much of this current is caused by an efflux of Cl . This implies that the neurons have one or more mechanisms for accumulating cytoplasmic Cl at rest. Whether odors activate an efflux of Cl in intact olfactory epithelium, where the ionic environment is poorly characterized, has not been previously determined. In mouse olfactory epithelium, we found that >80% of the summated electrical response to odors is blocked by niflumic acid or flufenamic acid, each of which inhibits Ca 2+ -activated Cl channels in ORNs. This indicates that ORNs accumulate Cl in situ. Recent evidence has shown that NKCC1, a Na + -K + -2Cl cotransporter, contributes to Cl accumulation in mammalian ORNs. However, we find that the epithelial response to odors is only reduced by 39% in mice carrying a null mutation in Nkcc1 . As in the wild-type, most of the response is blocked by niflumic acid or flufenamic acid, indicating that the underlying current is carried by Cl . We conclude that ORNs effectively accumulate Cl in situ even in the absence of NKCC1. The Cl -transport mechanism underlying this accumulation has not yet been identified.
Address for reprint requests and other correspondence: S. J. Kleene, Dept. of Cell Biology, Neurobiology, and Anatomy, Univ. of Cincinnati, PO Box 670667, Cincinnati, OH 45267-0667 (E-mail: steve{at}syrano.acb.uc.edu )</abstract><cop>United States</cop><pub>Am Phys Soc</pub><pmid>16319203</pmid><doi>10.1152/jn.00962.2005</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Animals Chlorine - metabolism Membrane Potentials - physiology Mice Olfactory Mucosa - physiology Olfactory Receptor Neurons - physiology Sodium-Potassium-Chloride Symporters - deficiency Solute Carrier Family 12, Member 2 |
title | Neuronal Chloride Accumulation in Olfactory Epithelium of Mice Lacking NKCC1 |
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