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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
1993-6-3
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pubmed:abstractText |
Percent recovery of CA1 field EPSP amplitude following various anoxic aglycemic (AA) periods was examined in rat hippocampal slices superfused with MK-801 (0.1 microM, 1 microM, 10 microM) or Mg(2+)-free artificial cerebrospinal fluid. Slices treated with 0.1 microM MK-801 showed greater percent recuperation of EPSP amplitude following 3 min 30 s of AA (36 +/- 12% vs 6 +/- 4% in controls). Higher concentrations of MK-801 resulted in a greater recovery of EPSP amplitudes in more than one time period of AA, with 10 microM MK-801 providing protection in up to 4 min 30 s AA. Percent recuperation of EPSP amplitude was smaller in Mg(2+)-free slices following 2 min (34 +/- 15% vs 81 +/- 11% in controls) and 2 min 30 (25 +/- 14% vs 77 +/- 10% in controls) of AA. These results suggest that the activation of the N-methyl-D-aspartate (NMDA) receptor channel may contribute to irreversible AA induced synaptic failure in CA1.
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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:month |
Apr
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
2
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pubmed:volume |
607
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
54-60
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8386976-Animals,
pubmed-meshheading:8386976-Anoxia,
pubmed-meshheading:8386976-Blood Glucose,
pubmed-meshheading:8386976-Dizocilpine Maleate,
pubmed-meshheading:8386976-Electrophysiology,
pubmed-meshheading:8386976-Evoked Potentials,
pubmed-meshheading:8386976-Hippocampus,
pubmed-meshheading:8386976-Magnesium,
pubmed-meshheading:8386976-Male,
pubmed-meshheading:8386976-Rats,
pubmed-meshheading:8386976-Rats, Wistar,
pubmed-meshheading:8386976-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:8386976-Synapses,
pubmed-meshheading:8386976-Synaptic Transmission
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pubmed:year |
1993
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pubmed:articleTitle |
The NMDA receptor contributes to anoxic aglycemic induced irreversible inhibition of synaptic transmission.
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pubmed:affiliation |
INSERM Unit 29, Paris, France.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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