Source:http://linkedlifedata.com/resource/pubmed/id/12428274
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2002-11-13
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pubmed:abstractText |
Effects of idiotypic and antiidiotypic antibodies against protein S100b on synaptic transmission and long-term potentiation of CA1 pyramidal neurons in rat hippocampus were studied. Idiotypic antibodies against protein S100b inhibited synaptic transmission from Schaffer collateral axons to pyramidal neurons, but had no effect on neuronal responses to antidromic stimulation. Antiidiotypic antibodies against protein S100b facilitated neuronal responses to orthodromic stimulation. Idiotypic antibodies against protein S100b suppressed changes in neuronal responses to orthodromic stimulation during long-term potentiation, while antiidiotypic antibodies facilitated these effects. Our findings suggest that the effects of idiotypic and antiidiotypic antibodies to protein S100b are associated with their regulatory influences on synaptic transmission. These mechanisms differ from mechanisms of synaptic plasticity involved in long-term potentiation.
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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 |
Feb
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pubmed:issn |
0007-4888
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
133
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
110-3
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12428274-Animals,
pubmed-meshheading:12428274-Antibodies,
pubmed-meshheading:12428274-Hippocampus,
pubmed-meshheading:12428274-Long-Term Potentiation,
pubmed-meshheading:12428274-Male,
pubmed-meshheading:12428274-Nerve Growth Factors,
pubmed-meshheading:12428274-Neurons,
pubmed-meshheading:12428274-Rats,
pubmed-meshheading:12428274-Rats, Wistar,
pubmed-meshheading:12428274-S100 Proteins,
pubmed-meshheading:12428274-Synaptic Transmission
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pubmed:year |
2002
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pubmed:articleTitle |
Effects of antibodies against protein S100b on synaptic transmission and long-term potentiation in CA-1 hippocampal neurons in rats.
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pubmed:affiliation |
P. K. Anokhin Institute of Normal Physiology, Russian Academy of Medical Sciences, Moscow.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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