NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron
Early in development, GABA and glycine exert excitatory action that turns to inhibition due to modification of the chloride equilibrium potential ( E Cl ) controlled by the KCC2 and NKCC1 transporters. This switch is thought to be due to a late expression of KCC2 associated with a NKCC1 down-regulat...
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| Veröffentlicht in: | The Journal of physiology 2008-02, Vol.586 (4), p.1059-1075 |
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| creator | Delpy, Alain Allain, Anne‐Emilie Meyrand, Pierre Branchereau, Pascal |
| description | Early in development, GABA and glycine exert excitatory action that turns to inhibition due to modification of the chloride
equilibrium potential ( E Cl ) controlled by the KCC2 and NKCC1 transporters. This switch is thought to be due to a late expression of KCC2 associated
with a NKCC1 down-regulation. Here, we show in mouse embryonic spinal cord that both KCC2 and NKCC1 are expressed and functional
early in development (E11.5âE13.5) when GABA A receptor activation induces strong excitatory action. After E15.5, a switch occurs rendering GABA unable to provide excitation.
At these subsequent stages, NKCC1 becomes both inactive and less abundant in motoneurons while KCC2 remains functional and
hyperpolarizes E Cl . In conclusion, in contrast to other systems, the cotransporters are concomitantly expressed early in the development of
the mouse spinal cord. Moreover, whereas NKCC1 follows a classical functional extinction, KCC2 is highly expressed throughout
both early and late embryonic life. |
| doi_str_mv | 10.1113/jphysiol.2007.146993 |
| format | Article |
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equilibrium potential ( E Cl ) controlled by the KCC2 and NKCC1 transporters. This switch is thought to be due to a late expression of KCC2 associated
with a NKCC1 down-regulation. Here, we show in mouse embryonic spinal cord that both KCC2 and NKCC1 are expressed and functional
early in development (E11.5âE13.5) when GABA A receptor activation induces strong excitatory action. After E15.5, a switch occurs rendering GABA unable to provide excitation.
At these subsequent stages, NKCC1 becomes both inactive and less abundant in motoneurons while KCC2 remains functional and
hyperpolarizes E Cl . In conclusion, in contrast to other systems, the cotransporters are concomitantly expressed early in the development of
the mouse spinal cord. Moreover, whereas NKCC1 follows a classical functional extinction, KCC2 is highly expressed throughout
both early and late embryonic life.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2007.146993</identifier><identifier>PMID: 18096599</identifier><language>eng</language><publisher>Oxford, UK: The Physiological Society</publisher><subject>Action Potentials - physiology ; Animals ; Biophysical Phenomena ; Biophysics ; Bumetanide - pharmacology ; Chlorides - metabolism ; Female ; Furosemide - pharmacology ; GABA Agonists - pharmacology ; Isonicotinic Acids - pharmacology ; K Cl- Cotransporters ; Mice ; Motor Neurons - drug effects ; Motor Neurons - metabolism ; Neuroscience ; Patch-Clamp Techniques ; Pregnancy ; Sodium Potassium Chloride Symporter Inhibitors - pharmacology ; Sodium-Potassium-Chloride Symporters - metabolism ; Solute Carrier Family 12, Member 2 ; Spinal Nerves - embryology ; Spinal Nerves - metabolism ; Symporters - metabolism</subject><ispartof>The Journal of physiology, 2008-02, Vol.586 (4), p.1059-1075</ispartof><rights>2008 The Journal of Physiology © 2008 The Physiological Society</rights><rights>2008 The Authors. Journal compilation © 2008 The Physiological Society 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5558-5faebcc201ab1a2cec209e21bd079347799056bffd5b2846af61c834c8bf27c83</citedby><cites>FETCH-LOGICAL-c5558-5faebcc201ab1a2cec209e21bd079347799056bffd5b2846af61c834c8bf27c83</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/PMC2375629/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375629/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1416,1432,27922,27923,45572,45573,46407,46831,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18096599$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Delpy, Alain</creatorcontrib><creatorcontrib>Allain, Anne‐Emilie</creatorcontrib><creatorcontrib>Meyrand, Pierre</creatorcontrib><creatorcontrib>Branchereau, Pascal</creatorcontrib><title>NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Early in development, GABA and glycine exert excitatory action that turns to inhibition due to modification of the chloride
equilibrium potential ( E Cl ) controlled by the KCC2 and NKCC1 transporters. This switch is thought to be due to a late expression of KCC2 associated
with a NKCC1 down-regulation. Here, we show in mouse embryonic spinal cord that both KCC2 and NKCC1 are expressed and functional
early in development (E11.5âE13.5) when GABA A receptor activation induces strong excitatory action. After E15.5, a switch occurs rendering GABA unable to provide excitation.
At these subsequent stages, NKCC1 becomes both inactive and less abundant in motoneurons while KCC2 remains functional and
hyperpolarizes E Cl . In conclusion, in contrast to other systems, the cotransporters are concomitantly expressed early in the development of
the mouse spinal cord. Moreover, whereas NKCC1 follows a classical functional extinction, KCC2 is highly expressed throughout
both early and late embryonic life.</description><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>Biophysical Phenomena</subject><subject>Biophysics</subject><subject>Bumetanide - pharmacology</subject><subject>Chlorides - metabolism</subject><subject>Female</subject><subject>Furosemide - pharmacology</subject><subject>GABA Agonists - pharmacology</subject><subject>Isonicotinic Acids - pharmacology</subject><subject>K Cl- Cotransporters</subject><subject>Mice</subject><subject>Motor Neurons - drug effects</subject><subject>Motor Neurons - metabolism</subject><subject>Neuroscience</subject><subject>Patch-Clamp Techniques</subject><subject>Pregnancy</subject><subject>Sodium Potassium Chloride Symporter Inhibitors - pharmacology</subject><subject>Sodium-Potassium-Chloride Symporters - metabolism</subject><subject>Solute Carrier Family 12, Member 2</subject><subject>Spinal Nerves - embryology</subject><subject>Spinal Nerves - metabolism</subject><subject>Symporters - metabolism</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EotPCGyCUFWKTwXbiJN4goVGhQAUsytpynJvmVo4d7GSqES-Phwx_O1a-Vs75fE8OIc8Y3TLGild303CI6O2WU1pvWVlJWTwgm-OQ17UsHpINpZznRS3YGTmP8Y5SVlApH5Mz1lBZCSk35Punj7sdy4yfg3Zx8mGGkKHTZsa9ntG7bHEdBIsQMxjbcPAOTdbBHqyfRnBz5vvMDNYH7CAfoUM9Q5cIA7b4048uG_0SIYtT4tp0mb2DJXj3hDzqtY3w9HRekK9vL292V_n153fvd2-ucyOEaHLRa2iN4ZTplmluII0SOGs7mmKWKaukomr7vhMtb8pK9xUzTVGapu15naYL8nrlTkubNjRp66CtmgKOOhyU16j-_eJwULd-r3j6dxWXCfDiBAj-2wJxViNGA9ZqBymaqmnBqrLhSViuQhN8jAH6348wqo6tqV-tqWNram0t2Z7_veAf06mmJJCr4B4tHP4Lqm4-fOF1cUz_cvUOeDvcYwC1qqM3CPNBiaZSZUIJWfwAyCy7iw</recordid><startdate>20080215</startdate><enddate>20080215</enddate><creator>Delpy, Alain</creator><creator>Allain, Anne‐Emilie</creator><creator>Meyrand, Pierre</creator><creator>Branchereau, Pascal</creator><general>The Physiological Society</general><general>Blackwell Publishing Ltd</general><general>Blackwell Science Inc</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20080215</creationdate><title>NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron</title><author>Delpy, Alain ; Allain, Anne‐Emilie ; Meyrand, Pierre ; Branchereau, Pascal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5558-5faebcc201ab1a2cec209e21bd079347799056bffd5b2846af61c834c8bf27c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Action Potentials - physiology</topic><topic>Animals</topic><topic>Biophysical Phenomena</topic><topic>Biophysics</topic><topic>Bumetanide - pharmacology</topic><topic>Chlorides - metabolism</topic><topic>Female</topic><topic>Furosemide - pharmacology</topic><topic>GABA Agonists - pharmacology</topic><topic>Isonicotinic Acids - pharmacology</topic><topic>K Cl- Cotransporters</topic><topic>Mice</topic><topic>Motor Neurons - drug effects</topic><topic>Motor Neurons - metabolism</topic><topic>Neuroscience</topic><topic>Patch-Clamp Techniques</topic><topic>Pregnancy</topic><topic>Sodium Potassium Chloride Symporter Inhibitors - pharmacology</topic><topic>Sodium-Potassium-Chloride Symporters - metabolism</topic><topic>Solute Carrier Family 12, Member 2</topic><topic>Spinal Nerves - embryology</topic><topic>Spinal Nerves - metabolism</topic><topic>Symporters - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Delpy, Alain</creatorcontrib><creatorcontrib>Allain, Anne‐Emilie</creatorcontrib><creatorcontrib>Meyrand, Pierre</creatorcontrib><creatorcontrib>Branchereau, Pascal</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Delpy, Alain</au><au>Allain, Anne‐Emilie</au><au>Meyrand, Pierre</au><au>Branchereau, Pascal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2008-02-15</date><risdate>2008</risdate><volume>586</volume><issue>4</issue><spage>1059</spage><epage>1075</epage><pages>1059-1075</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>Early in development, GABA and glycine exert excitatory action that turns to inhibition due to modification of the chloride
equilibrium potential ( E Cl ) controlled by the KCC2 and NKCC1 transporters. This switch is thought to be due to a late expression of KCC2 associated
with a NKCC1 down-regulation. Here, we show in mouse embryonic spinal cord that both KCC2 and NKCC1 are expressed and functional
early in development (E11.5âE13.5) when GABA A receptor activation induces strong excitatory action. After E15.5, a switch occurs rendering GABA unable to provide excitation.
At these subsequent stages, NKCC1 becomes both inactive and less abundant in motoneurons while KCC2 remains functional and
hyperpolarizes E Cl . In conclusion, in contrast to other systems, the cotransporters are concomitantly expressed early in the development of
the mouse spinal cord. Moreover, whereas NKCC1 follows a classical functional extinction, KCC2 is highly expressed throughout
both early and late embryonic life.</abstract><cop>Oxford, UK</cop><pub>The Physiological Society</pub><pmid>18096599</pmid><doi>10.1113/jphysiol.2007.146993</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; Wiley Free Content; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Action Potentials - physiology Animals Biophysical Phenomena Biophysics Bumetanide - pharmacology Chlorides - metabolism Female Furosemide - pharmacology GABA Agonists - pharmacology Isonicotinic Acids - pharmacology K Cl- Cotransporters Mice Motor Neurons - drug effects Motor Neurons - metabolism Neuroscience Patch-Clamp Techniques Pregnancy Sodium Potassium Chloride Symporter Inhibitors - pharmacology Sodium-Potassium-Chloride Symporters - metabolism Solute Carrier Family 12, Member 2 Spinal Nerves - embryology Spinal Nerves - metabolism Symporters - metabolism |
| title | NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron |
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