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rdf:type |
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lifeskim:mentions |
umls-concept:C0001613,
umls-concept:C0007776,
umls-concept:C0014544,
umls-concept:C0014653,
umls-concept:C0017067,
umls-concept:C0021792,
umls-concept:C0022655,
umls-concept:C0205097,
umls-concept:C0205098,
umls-concept:C0683598,
umls-concept:C1274040,
umls-concept:C1417833,
umls-concept:C1517945
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pubmed:issue |
12
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pubmed:dateCreated |
2011-3-24
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pubmed:abstractText |
In rodents, cortical interneurons originate from the medial ganglionic eminence (MGE) and caudal ganglionic eminence (CGE) according to precise temporal schedules. The mechanisms controlling the specification of CGE-derived interneurons and their role in cortical circuitry are still unknown. Here, we show that COUP-TFI expression becomes restricted to the dorsal MGE and CGE at embryonic day 13.5 in the basal telencephalon. Conditional loss of function of COUP-TFI in subventricular precursors and postmitotic cells leads to a decrease of late-born, CGE-derived, VIP (vasoactive intestinal peptide)- and CR (calretinin)-expressing bipolar cortical neurons, compensated by the concurrent increase of early-born MGE-derived, PV (parvalbumin)-expressing interneurons. Strikingly, COUP-TFI mutants are more resistant to pharmacologically induced seizures, a phenotype that is dependent on GABAergic signaling. Together, our data indicate that COUP-TFI controls the delicate balance between MGE- and CGE-derived cortical interneurons by regulating intermediate progenitor divisions and ultimately affecting the activity of the cortical inhibitory circuitry.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1529-2401
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pubmed:author |
pubmed-author:AndolfiGennaroG,
pubmed-author:ArlottaPaolaP,
pubmed-author:ArmentanoMariaM,
pubmed-author:De LeonibusElviraE,
pubmed-author:GazteluJose MJM,
pubmed-author:LodatoSimonaS,
pubmed-author:Menendez de la PridaLisetL,
pubmed-author:StuderMichèleM,
pubmed-author:TomassyGiulio SrubekGS,
pubmed-author:TouzotAudreyA,
pubmed-author:UzcateguiYoryani GYG
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pubmed:issnType |
Electronic
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pubmed:day |
23
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4650-62
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pubmed:meshHeading |
pubmed-meshheading:21430164-Animals,
pubmed-meshheading:21430164-Antimetabolites,
pubmed-meshheading:21430164-Bromodeoxyuridine,
pubmed-meshheading:21430164-COUP Transcription Factor I,
pubmed-meshheading:21430164-Cell Proliferation,
pubmed-meshheading:21430164-Cerebral Cortex,
pubmed-meshheading:21430164-Convulsants,
pubmed-meshheading:21430164-Drug Resistance,
pubmed-meshheading:21430164-Electroencephalography,
pubmed-meshheading:21430164-Electrophysiological Phenomena,
pubmed-meshheading:21430164-Epilepsy,
pubmed-meshheading:21430164-Immunohistochemistry,
pubmed-meshheading:21430164-In Situ Hybridization,
pubmed-meshheading:21430164-Interneurons,
pubmed-meshheading:21430164-Median Eminence,
pubmed-meshheading:21430164-Mice,
pubmed-meshheading:21430164-Mice, Inbred C57BL,
pubmed-meshheading:21430164-Mice, Knockout,
pubmed-meshheading:21430164-Nerve Net,
pubmed-meshheading:21430164-Receptors, GABA-A,
pubmed-meshheading:21430164-Receptors, GABA-B,
pubmed-meshheading:21430164-Telencephalon,
pubmed-meshheading:21430164-gamma-Aminobutyric Acid
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pubmed:year |
2011
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pubmed:articleTitle |
Loss of COUP-TFI alters the balance between caudal ganglionic eminence- and medial ganglionic eminence-derived cortical interneurons and results in resistance to epilepsy.
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pubmed:affiliation |
Telethon Institute of Genetics and Medicine, Developmental Disorders Program, and European School of Molecular Medicine, 80131 Naples, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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