Source:http://linkedlifedata.com/resource/pubmed/id/17652774
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2007-7-26
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pubmed:abstractText |
A voltage-dependent but Ca2+-independent regulation of N-methyl-D-aspartate (NMDA) receptor outward activity was studied at the single channel level using outside-out patches of cultured mouse cortical neurons. Unlike the inward activity associated with Ca2+ and Na+ influx, the NMDA receptor outward K+ conductance was unaffected by changes in Ca2+ concentration. Following a depolarizing pre-pulse, the single channel open probability (NP o), amplitude, and open duration of the NMDA inward current decreased, whereas the same pre-depolarization increased those parameters of the NMDA outward current (pre-pulse facilitation). The outward NP o was increased by the pre-pulse facilitation, disregarding Ca2+ changes. The voltage-current relationships of the inward and outward currents were shifted by the pre-depolarization toward opposite directions. The Src family kinase inhibitor, PP1, and the Src kinase antibody, but not the anti-Fyn antibody, blocked the pre-pulse facilitation of the NMDA outward activity. On the other hand, a hyperpolarizing pre-pulse showed no effect on NMDA inward currents but inhibited outward currents (pre-pulse depression). Application of Src kinase, but not Fyn kinase, prevented the pre-pulse depression. We additionally showed that a depolarization pre-pulse potentiated miniature excitatory synaptic currents (mEPSCs). The effect was blocked by application of the NMDA receptor antagonist AP-5 during depolarization. These data suggest a voltage-sensitive regulation of NMDA receptor channels mediated by Src kinase. The selective changes in the NMDA receptor-mediated K+ efflux may represent a physiological and pathophysiological plasticity at the receptor level in response to dynamic changes in the membrane potential of central neurons.
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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,
http://linkedlifedata.com/resource/pubmed/chemical/FYN protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-fyn,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neuropeptide Y,
http://linkedlifedata.com/resource/pubmed/chemical/neuropeptide Y4 receptor,
http://linkedlifedata.com/resource/pubmed/chemical/src-Family Kinases
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pubmed:status |
MEDLINE
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pubmed:issn |
1085-9195
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
47
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
257-70
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17652774-Animals,
pubmed-meshheading:17652774-Apoptosis,
pubmed-meshheading:17652774-Calcium,
pubmed-meshheading:17652774-Electrophysiology,
pubmed-meshheading:17652774-Membrane Potentials,
pubmed-meshheading:17652774-Mice,
pubmed-meshheading:17652774-Neurons,
pubmed-meshheading:17652774-Potassium,
pubmed-meshheading:17652774-Potassium Channels,
pubmed-meshheading:17652774-Probability,
pubmed-meshheading:17652774-Proto-Oncogene Proteins c-fyn,
pubmed-meshheading:17652774-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:17652774-Receptors, Neuropeptide Y,
pubmed-meshheading:17652774-Synaptic Transmission,
pubmed-meshheading:17652774-src-Family Kinases
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pubmed:year |
2007
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pubmed:articleTitle |
Voltage-dependent and Src-mediated regulation of NMDA receptor single channel outward currents in cortical neurons.
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pubmed:affiliation |
Department of Pharmaceutical Sciences, Medical University of South Carolina, 280 Calhoun Street, Charleston, SC 29425, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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