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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2009-5-15
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pubmed:abstractText |
Overexpression of GABA(B)R1a receptors in mice (R1a(+)) results in an atypical absence seizure phenotype characterized by 3- to 6-Hz slow spike-and-wave discharges (SSWDs), reduced synaptic plasticity, and cognitive impairment. Here we tested the hypothesis that increased R1 expression causes atypical absence epilepsy and is not subunit specific. GABA(B)R1b receptors were overexpressed in mouse forebrain (R1b(+)) and confirmed by immunoblot and (3)H-CGP54626A autoradiography. The R1b(+) mice showed a reduction in hippocampal long-term potentiation and GABA(A) receptor-mediated inhibitory postsynaptic currents. R1b(+) mice manifested an electrographic, pharmacological, and behavioral phenotype consistent with atypical absence seizures, though less robust than R1a(+) in terms of SSWD duration and severity of cognitive impairment. These results suggest that abnormal GABA(B)R1b function plays a lesser role in the development of atypical absence epilepsy.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/2-amino-5-phosphopentanoic acid,
http://linkedlifedata.com/resource/pubmed/chemical/6-Cyano-7-nitroquinoxaline-2,3-dione,
http://linkedlifedata.com/resource/pubmed/chemical/CGP 54626,
http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/GABA type B receptor, subunit 1,
http://linkedlifedata.com/resource/pubmed/chemical/Organophosphorus Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, GABA-B,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium,
http://linkedlifedata.com/resource/pubmed/chemical/Valine
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1525-5069
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
577-81
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pubmed:meshHeading |
pubmed-meshheading:19435582-6-Cyano-7-nitroquinoxaline-2,3-dione,
pubmed-meshheading:19435582-Animals,
pubmed-meshheading:19435582-Animals, Newborn,
pubmed-meshheading:19435582-Autoradiography,
pubmed-meshheading:19435582-Cognition Disorders,
pubmed-meshheading:19435582-Disease Models, Animal,
pubmed-meshheading:19435582-Electric Stimulation,
pubmed-meshheading:19435582-Electroencephalography,
pubmed-meshheading:19435582-Epilepsy, Absence,
pubmed-meshheading:19435582-Excitatory Amino Acid Antagonists,
pubmed-meshheading:19435582-Hippocampus,
pubmed-meshheading:19435582-Inhibitory Postsynaptic Potentials,
pubmed-meshheading:19435582-Long-Term Potentiation,
pubmed-meshheading:19435582-Maze Learning,
pubmed-meshheading:19435582-Mice,
pubmed-meshheading:19435582-Mice, Transgenic,
pubmed-meshheading:19435582-Neurons,
pubmed-meshheading:19435582-Organophosphorus Compounds,
pubmed-meshheading:19435582-Patch-Clamp Techniques,
pubmed-meshheading:19435582-Phenotype,
pubmed-meshheading:19435582-Protein Binding,
pubmed-meshheading:19435582-Receptors, GABA-B,
pubmed-meshheading:19435582-Tritium,
pubmed-meshheading:19435582-Valine
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pubmed:year |
2009
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pubmed:articleTitle |
Severity of atypical absence phenotype in GABAB transgenic mice is subunit specific.
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pubmed:affiliation |
Neurosciences and Mental Health Research Program, The Hospital for Sick Children, Toronto, ON, Canada.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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