Source:http://linkedlifedata.com/resource/pubmed/id/18077676
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
50
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| pubmed:dateCreated |
2007-12-13
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| pubmed:abstractText |
Whether the subunit composition of NMDA receptors (NMDARs) controls the direction of long-term plasticity is currently disputed. In the visual layers of NR2A-/- juvenile superior colliculus (SC), synapses lose miniature NMDAR currents, leaving NR2B-rich receptors in extrasynaptic regions. Compared with wild type (WT), evoked NMDAR currents in mutant neurons have slower rise and decay times and lower NMDAR/AMPAR current ratios. Moreover, NMDAR and L-type Ca2+ channel-dependent SC long-term potentiation (LTP) is absent in NR2A-/- cells, whereas both WT and mutant neurons show long-duration, low-frequency-induced, long-term depression (LLF-LTD) that is blocked by either AP-5, nimodipine, or Ro 25-6981 [R-(R,S)-alpha-(4-hydroxyphenyl)-beta-methyl-4-(phenylmethyl)-1-piperidine propranol]. Thus, NMDAR currents or signaling localized at the postsynaptic density are essential to SC NMDAR-dependent LTP, whereas extrasynaptic or NR2B-rich NMDARs are necessary for LLF-LTD. However, synaptic NMDARs as well as the NR2A subunit are missing in NR2A-/- mice. Therefore, NR2 subunit-specific ligand binding/channel properties and/or separate signaling pathways interacting with NMDARs at synaptic versus extrasynaptic receptors could underlie these results.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/NR2A NMDA receptor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, AMPA,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate
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| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
1529-2401
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
12
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| pubmed:volume |
27
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
13649-54
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| pubmed:meshHeading |
pubmed-meshheading:18077676-Age Factors,
pubmed-meshheading:18077676-Animals,
pubmed-meshheading:18077676-Calcium Channel Blockers,
pubmed-meshheading:18077676-Calcium Channels, L-Type,
pubmed-meshheading:18077676-Excitatory Amino Acid Antagonists,
pubmed-meshheading:18077676-Excitatory Postsynaptic Potentials,
pubmed-meshheading:18077676-Long-Term Potentiation,
pubmed-meshheading:18077676-Long-Term Synaptic Depression,
pubmed-meshheading:18077676-Mice,
pubmed-meshheading:18077676-Mice, Inbred C57BL,
pubmed-meshheading:18077676-Mice, Knockout,
pubmed-meshheading:18077676-Neurons,
pubmed-meshheading:18077676-Organ Culture Techniques,
pubmed-meshheading:18077676-Patch-Clamp Techniques,
pubmed-meshheading:18077676-Receptors, AMPA,
pubmed-meshheading:18077676-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:18077676-Signal Transduction,
pubmed-meshheading:18077676-Superior Colliculi,
pubmed-meshheading:18077676-Synapses
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| pubmed:year |
2007
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| pubmed:articleTitle |
NR2A-/- mice lack long-term potentiation but retain NMDA receptor and L-type Ca2+ channel-dependent long-term depression in the juvenile superior colliculus.
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| pubmed:affiliation |
The McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. jpzhao@mit.edu
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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