Source:http://linkedlifedata.com/resource/pubmed/id/18058824
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2008-2-27
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| pubmed:abstractText |
Rett syndrome is an autism-spectrum disorder caused by loss of function mutations within the gene encoding methyl CpG-binding protein 2 (MeCP2). While subtle decreases in synaptic plasticity have been detected within cortical and hippocampal neurons of Mecp2-null mice, only minimal information exists regarding how the loss of MeCP2 affects network activity in the brain. To address this issue, we compared the intrinsic network activities of Mecp2-null hippocampal slices derived from symptomatic mice to wild-type slices. Extracellular and whole-cell patch recordings revealed that although spontaneous, IPSP-based rhythmic activity is present in Mecp2-null slices; its frequency is significantly reduced from wild-type. This reduction was not associated with alterations in the gross electrophysiological properties of hippocampal neurons, but was associated with a decreased level of spontaneous glutamate receptor-mediated synaptic currents in hippocampal CA3 neurons. Paradoxically, however, repetitive sharp wave-like discharges were readily induced in the Mecp2-null hippocampal slices by a brief train of high-frequency stimulation commonly used to establish long-term potentiation at wild-type slices. Taken together, our data indicate that the Mecp2-null hippocampal CA3 circuit has diminished basal inhibitory rhythmic activity, which in turn renders the circuitry prone to hyperexcitability.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
1098-1063
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| pubmed:author | |
| pubmed:copyrightInfo |
(c) 2007 Wiley-Liss, Inc.
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| pubmed:issnType |
Electronic
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| pubmed:volume |
18
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
294-309
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| pubmed:meshHeading |
pubmed-meshheading:18058824-Action Potentials,
pubmed-meshheading:18058824-Animals,
pubmed-meshheading:18058824-Biological Clocks,
pubmed-meshheading:18058824-Cortical Synchronization,
pubmed-meshheading:18058824-DNA-Binding Proteins,
pubmed-meshheading:18058824-Electric Stimulation,
pubmed-meshheading:18058824-Female,
pubmed-meshheading:18058824-Glutamic Acid,
pubmed-meshheading:18058824-Hippocampus,
pubmed-meshheading:18058824-Inhibitory Postsynaptic Potentials,
pubmed-meshheading:18058824-Long-Term Potentiation,
pubmed-meshheading:18058824-Male,
pubmed-meshheading:18058824-Methyl-CpG-Binding Protein 2,
pubmed-meshheading:18058824-Mice,
pubmed-meshheading:18058824-Mice, Knockout,
pubmed-meshheading:18058824-Nerve Net,
pubmed-meshheading:18058824-Neural Inhibition,
pubmed-meshheading:18058824-Organ Culture Techniques,
pubmed-meshheading:18058824-Patch-Clamp Techniques,
pubmed-meshheading:18058824-Periodicity,
pubmed-meshheading:18058824-Rett Syndrome,
pubmed-meshheading:18058824-Synaptic Transmission
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| pubmed:year |
2008
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| pubmed:articleTitle |
The MeCP2-null mouse hippocampus displays altered basal inhibitory rhythms and is prone to hyperexcitability.
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| pubmed:affiliation |
Division of Fundamental Neurobiology, Toronto Western Research Institute, University Health Network, Toronto, Ontario, M5T 2S8, Canada.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|