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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2010-3-10
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pubmed:abstractText |
Despite considerable evidence for a critical role of neuroligin-1 in the specification of excitatory synapses, the cellular mechanisms and physiological roles of neuroligin-1 in mature neural circuits are poorly understood. In mutant mice deficient in neuroligin-1, or adult rats in which neuroligin-1 was depleted, we have found that neuroligin-1 stabilizes the NMDA receptors residing in the postsynaptic membrane of amygdala principal neurons, which allows for a normal range of NMDA receptor-mediated synaptic transmission. We observed marked decreases in NMDA receptor-mediated synaptic currents at afferent inputs to the amygdala of neuroligin-1 knockout mice. However, the knockout mice exhibited a significant impairment in spike-timing-dependent long-term potentiation (STD-LTP) at the thalamic but not the cortical inputs to the amygdala. Subsequent electrophysiological analyses indicated that STD-LTP in the cortical pathway is largely independent of activation of postsynaptic NMDA receptors. These findings suggest that neuroligin-1 can modulate, in a pathway-specific manner, synaptic plasticity in the amygdala circuits of adult animals, likely by regulating the abundance of postsynaptic NMDA receptors.
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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 |
1091-6490
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pubmed:author |
pubmed-author:AnKyongmanK,
pubmed-author:BaileyCraig HCH,
pubmed-author:ChoiYun-BeomYB,
pubmed-author:JeongA YoungAY,
pubmed-author:JungJung HoonJH,
pubmed-author:JungSang-YongSY,
pubmed-author:KandelEric RER,
pubmed-author:KimJoung-HunJH,
pubmed-author:KimJuhyunJ,
pubmed-author:KwonOh BinOB,
pubmed-author:LeeC JustinCJ
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pubmed:issnType |
Electronic
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pubmed:day |
9
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pubmed:volume |
107
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4710-5
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pubmed:dateRevised |
2010-9-10
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pubmed:meshHeading |
pubmed-meshheading:20176955-6-Cyano-7-nitroquinoxaline-2,3-dione,
pubmed-meshheading:20176955-Action Potentials,
pubmed-meshheading:20176955-Amygdala,
pubmed-meshheading:20176955-Animals,
pubmed-meshheading:20176955-Blotting, Western,
pubmed-meshheading:20176955-Cell Adhesion Molecules, Neuronal,
pubmed-meshheading:20176955-Cell Line,
pubmed-meshheading:20176955-Dizocilpine Maleate,
pubmed-meshheading:20176955-Excitatory Amino Acid Antagonists,
pubmed-meshheading:20176955-Excitatory Postsynaptic Potentials,
pubmed-meshheading:20176955-Humans,
pubmed-meshheading:20176955-Long-Term Potentiation,
pubmed-meshheading:20176955-Mice,
pubmed-meshheading:20176955-Mice, Knockout,
pubmed-meshheading:20176955-Neuronal Plasticity,
pubmed-meshheading:20176955-RNA Interference,
pubmed-meshheading:20176955-Rats,
pubmed-meshheading:20176955-Rats, Sprague-Dawley,
pubmed-meshheading:20176955-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:20176955-Synaptic Transmission,
pubmed-meshheading:20176955-Thalamus
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pubmed:year |
2010
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pubmed:articleTitle |
Input-specific synaptic plasticity in the amygdala is regulated by neuroligin-1 via postsynaptic NMDA receptors.
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pubmed:affiliation |
Department of Life Science, Pohang University of Science and Technology, Pohang, Gyungbuk 790-784, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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