Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity
Background: Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of i...
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| Veröffentlicht in: | Molecular pain 2014-01, Vol.10 (1), p.5-5 |
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| description | Background:
Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of ion channels in dorsal-root ganglion (DRG) neurons. Anoctamin 1 (ANO1/TMEM16A), a Ca2+ activated chloride channel is highly visible in small DRG neurons and responds to heat. Mice with an abolished function of ANO1 in DRG neurons demonstrated attenuated pain-like behaviors when exposed to noxious heat, suggesting a role in acute thermal nociception. In this study, we further examined the function of ANO1 in mediating inflammation- or injury-induced hyperalgesia or allodynia.
Results:
Using Advillin/Ano1fl/fl (Adv/Ano1fl/fl) mice that have a functional ablation of Ano1 mainly in DRG neurons, we were able to determine its role in mediating thermal hyperalgesia and mechanical allodynia induced by inflammation or nerve injury. The thermal hyperalgesia and mechanical allodynia induced by carrageenan injection and spared-nerve injury were significantly reduced in Adv/Ano1fl/fl mice. In addition, flinching or licking behavior after bradykinin or formalin injection was also significantly reduced in Adv/Ano1fl/fl mice. Since pathological conditions augment nociceptive behaviors, we expected ANO1's contribution to the excitability of DRG neurons. Indeed, the application of inflammatory mediators reduced the threshold for action potential (rheobase) or time for induction of the first action potential in DRG neurons isolated from control (Ano1fl/fl) mice. These parameters for neuronal excitability induced by inflammatory mediators were not changed in Adv/Ano1fl/fl mice, suggesting an active contribution of ANO1 in augmenting the neuronal excitability.
Conclusions:
In addition to ANO1's role in mediating acute thermal pain as a heat sensor, ANO1 is also capable of augmenting the excitability of DRG neurons under inflammatory or neuropathic conditions and thereby aggravates inflammation- or tissue injury-induced pathological pain. |
| doi_str_mv | 10.1186/1744-8069-10-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3929161</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1186_1744-8069-10-5</sage_id><sourcerecordid>1505338609</sourcerecordid><originalsourceid>FETCH-LOGICAL-b639t-2e98151780544a62e6e9d8de3f4695714abb493e2f3ac74719e6730e4a8726913</originalsourceid><addsrcrecordid>eNp9kktr3DAURkVpaNK02y6LoZtAcSJZL2tTGIY2GQgJhXYtZPs61WBLU0kemH9fmUmHSfpYSegejj4-LkLvCL4kpBZXRDJW1liokuCSv0Bnh4eXR_dT9DrGNcZUYkFeodOKMY4prs_Q14XzbTKjdQUplt6lYJspQSySL1auH8w4muTDrjCuK-4gbKFcufWUH1aum1roipvdBkIEF22yW5t2b9BJb4YIbx_Pc_T9y-dvy5vy9v56tVzclo2gKpUVqJpwImvMGTOiAgGqqzugPROKS8JM0zBFoeqpaSWTRIGQFAMztayEIvQcfdp7N1MzQtdCzm4GvQl2NGGnvbH66cTZH_rBbzVVlSJiFiz2gsb6fwieTlo_6rlSPVeqCdY8Oy4eQwT_c4KY9GhjC8NgHPgpasIxp7QWWGX0wzN07afgckW6UphLToRg_6OyC_PcHZupyz3VBh9jgP6QOqea9-LPnO-PyzrgvxchAx_3QDQPcPTn33W_AMRuv38</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1500563944</pqid></control><display><type>article</type><title>Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity</title><source>MEDLINE</source><source>Sage Journals GOLD Open Access 2024</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>Springer Nature OA Free Journals</source><creator>Lee, Byeongjun ; Cho, Hawon ; Jung, Jooyoung ; Yang, Young Duk ; Yang, Dong-Jin ; Oh, Uhtaek</creator><creatorcontrib>Lee, Byeongjun ; Cho, Hawon ; Jung, Jooyoung ; Yang, Young Duk ; Yang, Dong-Jin ; Oh, Uhtaek</creatorcontrib><description>Background:
Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of ion channels in dorsal-root ganglion (DRG) neurons. Anoctamin 1 (ANO1/TMEM16A), a Ca2+ activated chloride channel is highly visible in small DRG neurons and responds to heat. Mice with an abolished function of ANO1 in DRG neurons demonstrated attenuated pain-like behaviors when exposed to noxious heat, suggesting a role in acute thermal nociception. In this study, we further examined the function of ANO1 in mediating inflammation- or injury-induced hyperalgesia or allodynia.
Results:
Using Advillin/Ano1fl/fl (Adv/Ano1fl/fl) mice that have a functional ablation of Ano1 mainly in DRG neurons, we were able to determine its role in mediating thermal hyperalgesia and mechanical allodynia induced by inflammation or nerve injury. The thermal hyperalgesia and mechanical allodynia induced by carrageenan injection and spared-nerve injury were significantly reduced in Adv/Ano1fl/fl mice. In addition, flinching or licking behavior after bradykinin or formalin injection was also significantly reduced in Adv/Ano1fl/fl mice. Since pathological conditions augment nociceptive behaviors, we expected ANO1's contribution to the excitability of DRG neurons. Indeed, the application of inflammatory mediators reduced the threshold for action potential (rheobase) or time for induction of the first action potential in DRG neurons isolated from control (Ano1fl/fl) mice. These parameters for neuronal excitability induced by inflammatory mediators were not changed in Adv/Ano1fl/fl mice, suggesting an active contribution of ANO1 in augmenting the neuronal excitability.
Conclusions:
In addition to ANO1's role in mediating acute thermal pain as a heat sensor, ANO1 is also capable of augmenting the excitability of DRG neurons under inflammatory or neuropathic conditions and thereby aggravates inflammation- or tissue injury-induced pathological pain.</description><identifier>ISSN: 1744-8069</identifier><identifier>EISSN: 1744-8069</identifier><identifier>DOI: 10.1186/1744-8069-10-5</identifier><identifier>PMID: 24450308</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Action potential ; Animals ; Anoctamin-1 ; Behavior ; Body temperature ; Bradykinin ; Bradykinin - pharmacology ; Calcium chloride ; Chloride Channels - metabolism ; Colleges & universities ; Excitability ; Experiments ; Formaldehyde - pharmacology ; Gene Expression Regulation - drug effects ; Heat ; Hyperalgesia ; Hyperalgesia - etiology ; Hyperalgesia - genetics ; Hyperalgesia - pathology ; Hypersensitivity ; Hypersensitivity - etiology ; Hypersensitivity - genetics ; Hypersensitivity - pathology ; Inflammation ; Inflammation - complications ; Inflammation - genetics ; Inflammation - pathology ; Ion channels ; Laboratory animals ; Licking behavior ; Mice ; Mice, Knockout ; Molecular modelling ; Neurons ; Nociception - drug effects ; Organ Specificity - drug effects ; Pain ; Pain perception ; Pharmaceutical sciences ; Pharmacy ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Sciatic Nerve - drug effects ; Sciatic Nerve - injuries ; Sciatic Nerve - metabolism ; Sciatic Nerve - pathology</subject><ispartof>Molecular pain, 2014-01, Vol.10 (1), p.5-5</ispartof><rights>2014 Lee et al</rights><rights>2014 Lee et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>2014 Lee et al. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/2.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2014 Lee et al.; licensee BioMed Central Ltd. 2014 Lee et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b639t-2e98151780544a62e6e9d8de3f4695714abb493e2f3ac74719e6730e4a8726913</citedby><cites>FETCH-LOGICAL-b639t-2e98151780544a62e6e9d8de3f4695714abb493e2f3ac74719e6730e4a8726913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929161/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929161/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,21945,27830,27901,27902,44921,45309,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24450308$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Byeongjun</creatorcontrib><creatorcontrib>Cho, Hawon</creatorcontrib><creatorcontrib>Jung, Jooyoung</creatorcontrib><creatorcontrib>Yang, Young Duk</creatorcontrib><creatorcontrib>Yang, Dong-Jin</creatorcontrib><creatorcontrib>Oh, Uhtaek</creatorcontrib><title>Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity</title><title>Molecular pain</title><addtitle>Mol Pain</addtitle><description>Background:
Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of ion channels in dorsal-root ganglion (DRG) neurons. Anoctamin 1 (ANO1/TMEM16A), a Ca2+ activated chloride channel is highly visible in small DRG neurons and responds to heat. Mice with an abolished function of ANO1 in DRG neurons demonstrated attenuated pain-like behaviors when exposed to noxious heat, suggesting a role in acute thermal nociception. In this study, we further examined the function of ANO1 in mediating inflammation- or injury-induced hyperalgesia or allodynia.
Results:
Using Advillin/Ano1fl/fl (Adv/Ano1fl/fl) mice that have a functional ablation of Ano1 mainly in DRG neurons, we were able to determine its role in mediating thermal hyperalgesia and mechanical allodynia induced by inflammation or nerve injury. The thermal hyperalgesia and mechanical allodynia induced by carrageenan injection and spared-nerve injury were significantly reduced in Adv/Ano1fl/fl mice. In addition, flinching or licking behavior after bradykinin or formalin injection was also significantly reduced in Adv/Ano1fl/fl mice. Since pathological conditions augment nociceptive behaviors, we expected ANO1's contribution to the excitability of DRG neurons. Indeed, the application of inflammatory mediators reduced the threshold for action potential (rheobase) or time for induction of the first action potential in DRG neurons isolated from control (Ano1fl/fl) mice. These parameters for neuronal excitability induced by inflammatory mediators were not changed in Adv/Ano1fl/fl mice, suggesting an active contribution of ANO1 in augmenting the neuronal excitability.
Conclusions:
In addition to ANO1's role in mediating acute thermal pain as a heat sensor, ANO1 is also capable of augmenting the excitability of DRG neurons under inflammatory or neuropathic conditions and thereby aggravates inflammation- or tissue injury-induced pathological pain.</description><subject>Action potential</subject><subject>Animals</subject><subject>Anoctamin-1</subject><subject>Behavior</subject><subject>Body temperature</subject><subject>Bradykinin</subject><subject>Bradykinin - pharmacology</subject><subject>Calcium chloride</subject><subject>Chloride Channels - metabolism</subject><subject>Colleges & universities</subject><subject>Excitability</subject><subject>Experiments</subject><subject>Formaldehyde - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Heat</subject><subject>Hyperalgesia</subject><subject>Hyperalgesia - etiology</subject><subject>Hyperalgesia - genetics</subject><subject>Hyperalgesia - pathology</subject><subject>Hypersensitivity</subject><subject>Hypersensitivity - etiology</subject><subject>Hypersensitivity - genetics</subject><subject>Hypersensitivity - pathology</subject><subject>Inflammation</subject><subject>Inflammation - complications</subject><subject>Inflammation - genetics</subject><subject>Inflammation - pathology</subject><subject>Ion channels</subject><subject>Laboratory animals</subject><subject>Licking behavior</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Molecular modelling</subject><subject>Neurons</subject><subject>Nociception - drug effects</subject><subject>Organ Specificity - drug effects</subject><subject>Pain</subject><subject>Pain perception</subject><subject>Pharmaceutical sciences</subject><subject>Pharmacy</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Sciatic Nerve - drug effects</subject><subject>Sciatic Nerve - injuries</subject><subject>Sciatic Nerve - metabolism</subject><subject>Sciatic Nerve - pathology</subject><issn>1744-8069</issn><issn>1744-8069</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kktr3DAURkVpaNK02y6LoZtAcSJZL2tTGIY2GQgJhXYtZPs61WBLU0kemH9fmUmHSfpYSegejj4-LkLvCL4kpBZXRDJW1liokuCSv0Bnh4eXR_dT9DrGNcZUYkFeodOKMY4prs_Q14XzbTKjdQUplt6lYJspQSySL1auH8w4muTDrjCuK-4gbKFcufWUH1aum1roipvdBkIEF22yW5t2b9BJb4YIbx_Pc_T9y-dvy5vy9v56tVzclo2gKpUVqJpwImvMGTOiAgGqqzugPROKS8JM0zBFoeqpaSWTRIGQFAMztayEIvQcfdp7N1MzQtdCzm4GvQl2NGGnvbH66cTZH_rBbzVVlSJiFiz2gsb6fwieTlo_6rlSPVeqCdY8Oy4eQwT_c4KY9GhjC8NgHPgpasIxp7QWWGX0wzN07afgckW6UphLToRg_6OyC_PcHZupyz3VBh9jgP6QOqea9-LPnO-PyzrgvxchAx_3QDQPcPTn33W_AMRuv38</recordid><startdate>20140123</startdate><enddate>20140123</enddate><creator>Lee, Byeongjun</creator><creator>Cho, Hawon</creator><creator>Jung, Jooyoung</creator><creator>Yang, Young Duk</creator><creator>Yang, Dong-Jin</creator><creator>Oh, Uhtaek</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>AFRWT</scope><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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20140123</creationdate><title>Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity</title><author>Lee, Byeongjun ; Cho, Hawon ; Jung, Jooyoung ; Yang, Young Duk ; Yang, Dong-Jin ; Oh, Uhtaek</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b639t-2e98151780544a62e6e9d8de3f4695714abb493e2f3ac74719e6730e4a8726913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Action potential</topic><topic>Animals</topic><topic>Anoctamin-1</topic><topic>Behavior</topic><topic>Body temperature</topic><topic>Bradykinin</topic><topic>Bradykinin - pharmacology</topic><topic>Calcium chloride</topic><topic>Chloride Channels - metabolism</topic><topic>Colleges & universities</topic><topic>Excitability</topic><topic>Experiments</topic><topic>Formaldehyde - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Heat</topic><topic>Hyperalgesia</topic><topic>Hyperalgesia - etiology</topic><topic>Hyperalgesia - genetics</topic><topic>Hyperalgesia - pathology</topic><topic>Hypersensitivity</topic><topic>Hypersensitivity - etiology</topic><topic>Hypersensitivity - genetics</topic><topic>Hypersensitivity - pathology</topic><topic>Inflammation</topic><topic>Inflammation - complications</topic><topic>Inflammation - genetics</topic><topic>Inflammation - pathology</topic><topic>Ion channels</topic><topic>Laboratory animals</topic><topic>Licking behavior</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Molecular modelling</topic><topic>Neurons</topic><topic>Nociception - drug effects</topic><topic>Organ Specificity - drug effects</topic><topic>Pain</topic><topic>Pain perception</topic><topic>Pharmaceutical sciences</topic><topic>Pharmacy</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Sciatic Nerve - drug effects</topic><topic>Sciatic Nerve - injuries</topic><topic>Sciatic Nerve - metabolism</topic><topic>Sciatic Nerve - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Byeongjun</creatorcontrib><creatorcontrib>Cho, Hawon</creatorcontrib><creatorcontrib>Jung, Jooyoung</creatorcontrib><creatorcontrib>Yang, Young Duk</creatorcontrib><creatorcontrib>Yang, Dong-Jin</creatorcontrib><creatorcontrib>Oh, Uhtaek</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular pain</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Byeongjun</au><au>Cho, Hawon</au><au>Jung, Jooyoung</au><au>Yang, Young Duk</au><au>Yang, Dong-Jin</au><au>Oh, Uhtaek</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity</atitle><jtitle>Molecular pain</jtitle><addtitle>Mol Pain</addtitle><date>2014-01-23</date><risdate>2014</risdate><volume>10</volume><issue>1</issue><spage>5</spage><epage>5</epage><pages>5-5</pages><issn>1744-8069</issn><eissn>1744-8069</eissn><abstract>Background:
Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of ion channels in dorsal-root ganglion (DRG) neurons. Anoctamin 1 (ANO1/TMEM16A), a Ca2+ activated chloride channel is highly visible in small DRG neurons and responds to heat. Mice with an abolished function of ANO1 in DRG neurons demonstrated attenuated pain-like behaviors when exposed to noxious heat, suggesting a role in acute thermal nociception. In this study, we further examined the function of ANO1 in mediating inflammation- or injury-induced hyperalgesia or allodynia.
Results:
Using Advillin/Ano1fl/fl (Adv/Ano1fl/fl) mice that have a functional ablation of Ano1 mainly in DRG neurons, we were able to determine its role in mediating thermal hyperalgesia and mechanical allodynia induced by inflammation or nerve injury. The thermal hyperalgesia and mechanical allodynia induced by carrageenan injection and spared-nerve injury were significantly reduced in Adv/Ano1fl/fl mice. In addition, flinching or licking behavior after bradykinin or formalin injection was also significantly reduced in Adv/Ano1fl/fl mice. Since pathological conditions augment nociceptive behaviors, we expected ANO1's contribution to the excitability of DRG neurons. Indeed, the application of inflammatory mediators reduced the threshold for action potential (rheobase) or time for induction of the first action potential in DRG neurons isolated from control (Ano1fl/fl) mice. These parameters for neuronal excitability induced by inflammatory mediators were not changed in Adv/Ano1fl/fl mice, suggesting an active contribution of ANO1 in augmenting the neuronal excitability.
Conclusions:
In addition to ANO1's role in mediating acute thermal pain as a heat sensor, ANO1 is also capable of augmenting the excitability of DRG neurons under inflammatory or neuropathic conditions and thereby aggravates inflammation- or tissue injury-induced pathological pain.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>24450308</pmid><doi>10.1186/1744-8069-10-5</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Action potential Animals Anoctamin-1 Behavior Body temperature Bradykinin Bradykinin - pharmacology Calcium chloride Chloride Channels - metabolism Colleges & universities Excitability Experiments Formaldehyde - pharmacology Gene Expression Regulation - drug effects Heat Hyperalgesia Hyperalgesia - etiology Hyperalgesia - genetics Hyperalgesia - pathology Hypersensitivity Hypersensitivity - etiology Hypersensitivity - genetics Hypersensitivity - pathology Inflammation Inflammation - complications Inflammation - genetics Inflammation - pathology Ion channels Laboratory animals Licking behavior Mice Mice, Knockout Molecular modelling Neurons Nociception - drug effects Organ Specificity - drug effects Pain Pain perception Pharmaceutical sciences Pharmacy RNA, Messenger - genetics RNA, Messenger - metabolism Sciatic Nerve - drug effects Sciatic Nerve - injuries Sciatic Nerve - metabolism Sciatic Nerve - pathology |
| title | Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity |
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