Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2
In healthy adults, activation of γ-aminobutyric acid (GABA) A and glycine receptors inhibits neurons as a result of low intracellular chloride concentration ([Cl –] ᵢ), which is maintained by the potassium-chloride cotransporter KCC2. A reduction of KCC2 expression or function is implicated in the p...
Gespeichert in:
| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2013-01, Vol.110 (1), p.348-353 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 353 |
|---|---|
| container_issue | 1 |
| container_start_page | 348 |
| container_title | Proceedings of the National Academy of Sciences - PNAS |
| container_volume | 110 |
| creator | Bos, Rémi Sadlaoud, Karina Boulenguez, Pascale Buttigieg, Dorothée Liabeuf, Sylvie Brocard, Cécile Haase, Georg Bras, Hélène Vinay, Laurent |
| description | In healthy adults, activation of γ-aminobutyric acid (GABA) A and glycine receptors inhibits neurons as a result of low intracellular chloride concentration ([Cl –] ᵢ), which is maintained by the potassium-chloride cotransporter KCC2. A reduction of KCC2 expression or function is implicated in the pathogenesis of several neurological disorders, including spasticity and chronic pain following spinal cord injury (SCI). Given the critical role of KCC2 in regulating the strength and robustness of inhibition, identifying tools that may increase KCC2 function and, hence, restore endogenous inhibition in pathological conditions is of particular importance. We show that activation of 5-hydroxytryptamine (5-HT) type 2A receptors to serotonin hyperpolarizes the reversal potential of inhibitory postsynaptic potentials (IPSPs), E IPSP, in spinal motoneurons, increases the cell membrane expression of KCC2 and both restores endogenous inhibition and reduces spasticity after SCI in rats. Up-regulation of KCC2 function by targeting 5-HT ₂A receptors, therefore, has therapeutic potential in the treatment of neurological disorders involving altered chloride homeostasis. However, these receptors have been implicated in several psychiatric disorders, and their effects on pain processing are controversial, highlighting the need to further investigate the potential systemic effects of specific 5-HT ₂AR agonists, such as (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl)methylamine hydrobromide (TCB-2). |
| doi_str_mv | 10.1073/pnas.1213680110 |
| format | Article |
| fullrecord | <record><control><sourceid>jstor_pubme</sourceid><recordid>TN_cdi_pubmed_primary_23248270</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><jstor_id>42553943</jstor_id><sourcerecordid>42553943</sourcerecordid><originalsourceid>FETCH-LOGICAL-c622t-8a6be781e506c6a752150eb8472deda9dfddd96cfa6b75a0df121edd09d9e8553</originalsourceid><addsrcrecordid>eNpdkc1vEzEQxS0EomnhzAlYiQscth1_ey9IUVQIaiQOtGfLsb3JRpv1Yu9G4r_Hq6Qp9GTZ7zfPM_MQeofhGoOkN31n0jUmmAoFGMMLNMNQ4VKwCl6iGQCRpWKEXaDLlHYAUHEFr9EFoYQpImGG9NwOzcEMTeiKUBe8XN6TeRG99f0QYirGPvrN2JrBp2LY-qIeO_sIT_fOjzF0pi3uykVb2DBE06U-xMHH4m6xIG_Qq9q0yb89nVfo4dvt_WJZrn5-_7GYr0orCBlKZcTaS4U9B2GFkZxgDn6tmCTOO1O52jlXCVtnTnIDrs5De-egcpVXnNMr9PXo24_rvXfWd7mTVvex2Zv4RwfT6P-VrtnqTThoyqnC1WTw5WiwfVa2nK_09AYkr49yccCZ_Xz6LIbfo0-D3jfJ-rY1nQ9j0lgBxSCohIx-eobuwhjzwjJFhGCUgWSZujlSNoaUoq_PHWDQU9B6Clo_BZ0rPvw775l_TDYD70_AVHm2m_w0ZepJ36Uc9BlgJC-zYjTrH496bYI2m9gk_fCLABYAOG9MCvoX3gjAMw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1266434074</pqid></control><display><type>article</type><title>Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2</title><source>Jstor Complete Legacy</source><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Bos, Rémi ; Sadlaoud, Karina ; Boulenguez, Pascale ; Buttigieg, Dorothée ; Liabeuf, Sylvie ; Brocard, Cécile ; Haase, Georg ; Bras, Hélène ; Vinay, Laurent</creator><creatorcontrib>Bos, Rémi ; Sadlaoud, Karina ; Boulenguez, Pascale ; Buttigieg, Dorothée ; Liabeuf, Sylvie ; Brocard, Cécile ; Haase, Georg ; Bras, Hélène ; Vinay, Laurent</creatorcontrib><description>In healthy adults, activation of γ-aminobutyric acid (GABA) A and glycine receptors inhibits neurons as a result of low intracellular chloride concentration ([Cl –] ᵢ), which is maintained by the potassium-chloride cotransporter KCC2. A reduction of KCC2 expression or function is implicated in the pathogenesis of several neurological disorders, including spasticity and chronic pain following spinal cord injury (SCI). Given the critical role of KCC2 in regulating the strength and robustness of inhibition, identifying tools that may increase KCC2 function and, hence, restore endogenous inhibition in pathological conditions is of particular importance. We show that activation of 5-hydroxytryptamine (5-HT) type 2A receptors to serotonin hyperpolarizes the reversal potential of inhibitory postsynaptic potentials (IPSPs), E IPSP, in spinal motoneurons, increases the cell membrane expression of KCC2 and both restores endogenous inhibition and reduces spasticity after SCI in rats. Up-regulation of KCC2 function by targeting 5-HT ₂A receptors, therefore, has therapeutic potential in the treatment of neurological disorders involving altered chloride homeostasis. However, these receptors have been implicated in several psychiatric disorders, and their effects on pain processing are controversial, highlighting the need to further investigate the potential systemic effects of specific 5-HT ₂AR agonists, such as (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl)methylamine hydrobromide (TCB-2).</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1213680110</identifier><identifier>PMID: 23248270</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>adults ; agonists ; animal injuries ; Animals ; behavior disorders ; Behavioral neuroscience ; Biological Sciences ; Blotting, Western ; Bridged Bicyclo Compounds - pharmacology ; Cell membranes ; Chlorides ; Chlorides - metabolism ; gamma-aminobutyric acid ; Gene expression ; Gene Expression Regulation - drug effects ; H-Reflex ; Homeostasis ; Immunohistochemistry ; Inhibitory Postsynaptic Potentials - physiology ; K Cl- Cotransporters ; Life Sciences ; methylamine ; Methylamines - pharmacology ; motor neurons ; Motor Neurons - metabolism ; Muscle Spasticity - drug therapy ; Muscle Spasticity - etiology ; nervous system diseases ; Neurobiology ; Neurochemistry ; Neurological disorders ; Neurons ; Neurons and Cognition ; Pain ; pathogenesis ; Pathology ; potassium chloride ; Proteins ; Rats ; Receptor, Serotonin, 5-HT2A - metabolism ; Receptors ; Serotonin ; Serotonin - metabolism ; Serotonin - pharmacology ; Serotonin 5-HT2 Receptor Agonists - pharmacology ; Serotonin receptors ; Spinal cord ; Spinal Cord Injuries - complications ; Spinal Nerve roots ; symporters ; Symporters - metabolism</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2013-01, Vol.110 (1), p.348-353</ispartof><rights>copyright © 1993-2008 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Jan 2, 2013</rights><rights>Attribution</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c622t-8a6be781e506c6a752150eb8472deda9dfddd96cfa6b75a0df121edd09d9e8553</citedby><cites>FETCH-LOGICAL-c622t-8a6be781e506c6a752150eb8472deda9dfddd96cfa6b75a0df121edd09d9e8553</cites><orcidid>0000-0001-5384-9006 ; 0000-0003-2639-3271</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/110/1.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/42553943$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/42553943$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23248270$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://amu.hal.science/hal-02009356$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Bos, Rémi</creatorcontrib><creatorcontrib>Sadlaoud, Karina</creatorcontrib><creatorcontrib>Boulenguez, Pascale</creatorcontrib><creatorcontrib>Buttigieg, Dorothée</creatorcontrib><creatorcontrib>Liabeuf, Sylvie</creatorcontrib><creatorcontrib>Brocard, Cécile</creatorcontrib><creatorcontrib>Haase, Georg</creatorcontrib><creatorcontrib>Bras, Hélène</creatorcontrib><creatorcontrib>Vinay, Laurent</creatorcontrib><title>Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>In healthy adults, activation of γ-aminobutyric acid (GABA) A and glycine receptors inhibits neurons as a result of low intracellular chloride concentration ([Cl –] ᵢ), which is maintained by the potassium-chloride cotransporter KCC2. A reduction of KCC2 expression or function is implicated in the pathogenesis of several neurological disorders, including spasticity and chronic pain following spinal cord injury (SCI). Given the critical role of KCC2 in regulating the strength and robustness of inhibition, identifying tools that may increase KCC2 function and, hence, restore endogenous inhibition in pathological conditions is of particular importance. We show that activation of 5-hydroxytryptamine (5-HT) type 2A receptors to serotonin hyperpolarizes the reversal potential of inhibitory postsynaptic potentials (IPSPs), E IPSP, in spinal motoneurons, increases the cell membrane expression of KCC2 and both restores endogenous inhibition and reduces spasticity after SCI in rats. Up-regulation of KCC2 function by targeting 5-HT ₂A receptors, therefore, has therapeutic potential in the treatment of neurological disorders involving altered chloride homeostasis. However, these receptors have been implicated in several psychiatric disorders, and their effects on pain processing are controversial, highlighting the need to further investigate the potential systemic effects of specific 5-HT ₂AR agonists, such as (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl)methylamine hydrobromide (TCB-2).</description><subject>adults</subject><subject>agonists</subject><subject>animal injuries</subject><subject>Animals</subject><subject>behavior disorders</subject><subject>Behavioral neuroscience</subject><subject>Biological Sciences</subject><subject>Blotting, Western</subject><subject>Bridged Bicyclo Compounds - pharmacology</subject><subject>Cell membranes</subject><subject>Chlorides</subject><subject>Chlorides - metabolism</subject><subject>gamma-aminobutyric acid</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>H-Reflex</subject><subject>Homeostasis</subject><subject>Immunohistochemistry</subject><subject>Inhibitory Postsynaptic Potentials - physiology</subject><subject>K Cl- Cotransporters</subject><subject>Life Sciences</subject><subject>methylamine</subject><subject>Methylamines - pharmacology</subject><subject>motor neurons</subject><subject>Motor Neurons - metabolism</subject><subject>Muscle Spasticity - drug therapy</subject><subject>Muscle Spasticity - etiology</subject><subject>nervous system diseases</subject><subject>Neurobiology</subject><subject>Neurochemistry</subject><subject>Neurological disorders</subject><subject>Neurons</subject><subject>Neurons and Cognition</subject><subject>Pain</subject><subject>pathogenesis</subject><subject>Pathology</subject><subject>potassium chloride</subject><subject>Proteins</subject><subject>Rats</subject><subject>Receptor, Serotonin, 5-HT2A - metabolism</subject><subject>Receptors</subject><subject>Serotonin</subject><subject>Serotonin - metabolism</subject><subject>Serotonin - pharmacology</subject><subject>Serotonin 5-HT2 Receptor Agonists - pharmacology</subject><subject>Serotonin receptors</subject><subject>Spinal cord</subject><subject>Spinal Cord Injuries - complications</subject><subject>Spinal Nerve roots</subject><subject>symporters</subject><subject>Symporters - metabolism</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1vEzEQxS0EomnhzAlYiQscth1_ey9IUVQIaiQOtGfLsb3JRpv1Yu9G4r_Hq6Qp9GTZ7zfPM_MQeofhGoOkN31n0jUmmAoFGMMLNMNQ4VKwCl6iGQCRpWKEXaDLlHYAUHEFr9EFoYQpImGG9NwOzcEMTeiKUBe8XN6TeRG99f0QYirGPvrN2JrBp2LY-qIeO_sIT_fOjzF0pi3uykVb2DBE06U-xMHH4m6xIG_Qq9q0yb89nVfo4dvt_WJZrn5-_7GYr0orCBlKZcTaS4U9B2GFkZxgDn6tmCTOO1O52jlXCVtnTnIDrs5De-egcpVXnNMr9PXo24_rvXfWd7mTVvex2Zv4RwfT6P-VrtnqTThoyqnC1WTw5WiwfVa2nK_09AYkr49yccCZ_Xz6LIbfo0-D3jfJ-rY1nQ9j0lgBxSCohIx-eobuwhjzwjJFhGCUgWSZujlSNoaUoq_PHWDQU9B6Clo_BZ0rPvw775l_TDYD70_AVHm2m_w0ZepJ36Uc9BlgJC-zYjTrH496bYI2m9gk_fCLABYAOG9MCvoX3gjAMw</recordid><startdate>20130102</startdate><enddate>20130102</enddate><creator>Bos, Rémi</creator><creator>Sadlaoud, Karina</creator><creator>Boulenguez, Pascale</creator><creator>Buttigieg, Dorothée</creator><creator>Liabeuf, Sylvie</creator><creator>Brocard, Cécile</creator><creator>Haase, Georg</creator><creator>Bras, Hélène</creator><creator>Vinay, Laurent</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5384-9006</orcidid><orcidid>https://orcid.org/0000-0003-2639-3271</orcidid></search><sort><creationdate>20130102</creationdate><title>Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2</title><author>Bos, Rémi ; Sadlaoud, Karina ; Boulenguez, Pascale ; Buttigieg, Dorothée ; Liabeuf, Sylvie ; Brocard, Cécile ; Haase, Georg ; Bras, Hélène ; Vinay, Laurent</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c622t-8a6be781e506c6a752150eb8472deda9dfddd96cfa6b75a0df121edd09d9e8553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>adults</topic><topic>agonists</topic><topic>animal injuries</topic><topic>Animals</topic><topic>behavior disorders</topic><topic>Behavioral neuroscience</topic><topic>Biological Sciences</topic><topic>Blotting, Western</topic><topic>Bridged Bicyclo Compounds - pharmacology</topic><topic>Cell membranes</topic><topic>Chlorides</topic><topic>Chlorides - metabolism</topic><topic>gamma-aminobutyric acid</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>H-Reflex</topic><topic>Homeostasis</topic><topic>Immunohistochemistry</topic><topic>Inhibitory Postsynaptic Potentials - physiology</topic><topic>K Cl- Cotransporters</topic><topic>Life Sciences</topic><topic>methylamine</topic><topic>Methylamines - pharmacology</topic><topic>motor neurons</topic><topic>Motor Neurons - metabolism</topic><topic>Muscle Spasticity - drug therapy</topic><topic>Muscle Spasticity - etiology</topic><topic>nervous system diseases</topic><topic>Neurobiology</topic><topic>Neurochemistry</topic><topic>Neurological disorders</topic><topic>Neurons</topic><topic>Neurons and Cognition</topic><topic>Pain</topic><topic>pathogenesis</topic><topic>Pathology</topic><topic>potassium chloride</topic><topic>Proteins</topic><topic>Rats</topic><topic>Receptor, Serotonin, 5-HT2A - metabolism</topic><topic>Receptors</topic><topic>Serotonin</topic><topic>Serotonin - metabolism</topic><topic>Serotonin - pharmacology</topic><topic>Serotonin 5-HT2 Receptor Agonists - pharmacology</topic><topic>Serotonin receptors</topic><topic>Spinal cord</topic><topic>Spinal Cord Injuries - complications</topic><topic>Spinal Nerve roots</topic><topic>symporters</topic><topic>Symporters - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bos, Rémi</creatorcontrib><creatorcontrib>Sadlaoud, Karina</creatorcontrib><creatorcontrib>Boulenguez, Pascale</creatorcontrib><creatorcontrib>Buttigieg, Dorothée</creatorcontrib><creatorcontrib>Liabeuf, Sylvie</creatorcontrib><creatorcontrib>Brocard, Cécile</creatorcontrib><creatorcontrib>Haase, Georg</creatorcontrib><creatorcontrib>Bras, Hélène</creatorcontrib><creatorcontrib>Vinay, Laurent</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bos, Rémi</au><au>Sadlaoud, Karina</au><au>Boulenguez, Pascale</au><au>Buttigieg, Dorothée</au><au>Liabeuf, Sylvie</au><au>Brocard, Cécile</au><au>Haase, Georg</au><au>Bras, Hélène</au><au>Vinay, Laurent</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2013-01-02</date><risdate>2013</risdate><volume>110</volume><issue>1</issue><spage>348</spage><epage>353</epage><pages>348-353</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>In healthy adults, activation of γ-aminobutyric acid (GABA) A and glycine receptors inhibits neurons as a result of low intracellular chloride concentration ([Cl –] ᵢ), which is maintained by the potassium-chloride cotransporter KCC2. A reduction of KCC2 expression or function is implicated in the pathogenesis of several neurological disorders, including spasticity and chronic pain following spinal cord injury (SCI). Given the critical role of KCC2 in regulating the strength and robustness of inhibition, identifying tools that may increase KCC2 function and, hence, restore endogenous inhibition in pathological conditions is of particular importance. We show that activation of 5-hydroxytryptamine (5-HT) type 2A receptors to serotonin hyperpolarizes the reversal potential of inhibitory postsynaptic potentials (IPSPs), E IPSP, in spinal motoneurons, increases the cell membrane expression of KCC2 and both restores endogenous inhibition and reduces spasticity after SCI in rats. Up-regulation of KCC2 function by targeting 5-HT ₂A receptors, therefore, has therapeutic potential in the treatment of neurological disorders involving altered chloride homeostasis. However, these receptors have been implicated in several psychiatric disorders, and their effects on pain processing are controversial, highlighting the need to further investigate the potential systemic effects of specific 5-HT ₂AR agonists, such as (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl)methylamine hydrobromide (TCB-2).</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>23248270</pmid><doi>10.1073/pnas.1213680110</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0001-5384-9006</orcidid><orcidid>https://orcid.org/0000-0003-2639-3271</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0027-8424 |
| ispartof | Proceedings of the National Academy of Sciences - PNAS, 2013-01, Vol.110 (1), p.348-353 |
| issn | 0027-8424 1091-6490 |
| language | eng |
| recordid | cdi_pubmed_primary_23248270 |
| source | Jstor Complete Legacy; MEDLINE; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | adults agonists animal injuries Animals behavior disorders Behavioral neuroscience Biological Sciences Blotting, Western Bridged Bicyclo Compounds - pharmacology Cell membranes Chlorides Chlorides - metabolism gamma-aminobutyric acid Gene expression Gene Expression Regulation - drug effects H-Reflex Homeostasis Immunohistochemistry Inhibitory Postsynaptic Potentials - physiology K Cl- Cotransporters Life Sciences methylamine Methylamines - pharmacology motor neurons Motor Neurons - metabolism Muscle Spasticity - drug therapy Muscle Spasticity - etiology nervous system diseases Neurobiology Neurochemistry Neurological disorders Neurons Neurons and Cognition Pain pathogenesis Pathology potassium chloride Proteins Rats Receptor, Serotonin, 5-HT2A - metabolism Receptors Serotonin Serotonin - metabolism Serotonin - pharmacology Serotonin 5-HT2 Receptor Agonists - pharmacology Serotonin receptors Spinal cord Spinal Cord Injuries - complications Spinal Nerve roots symporters Symporters - metabolism |
| title | Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T10%3A06%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-jstor_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Activation%20of%205-HT2A%20receptors%20upregulates%20the%20function%20of%20the%20neuronal%20K-Cl%20cotransporter%20KCC2&rft.jtitle=Proceedings%20of%20the%20National%20Academy%20of%20Sciences%20-%20PNAS&rft.au=Bos,%20R%C3%A9mi&rft.date=2013-01-02&rft.volume=110&rft.issue=1&rft.spage=348&rft.epage=353&rft.pages=348-353&rft.issn=0027-8424&rft.eissn=1091-6490&rft_id=info:doi/10.1073/pnas.1213680110&rft_dat=%3Cjstor_pubme%3E42553943%3C/jstor_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1266434074&rft_id=info:pmid/23248270&rft_jstor_id=42553943&rfr_iscdi=true |