Source:http://linkedlifedata.com/resource/pubmed/id/20804002
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-8-31
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pubmed:abstractText |
The path-clamp method used within the whole-cell configuration in experiments with convoluted medullar oblongata sections obtained from white mongrel male rats aged 13 to 17 days evidenced that 5 mV of mexidol caused 96 +/- 2% inhibition of the excitation postsynaptic current in neurons of the medial vestibular nucleus generated by the depolarization step of 10 mV (holding potential = -70 my). This means that the antimotion sickness effect of mexidol has its origin in the ion mechanisms with involvement of the glutamate- and GABAergic components, primarily inhibition of ion currents through channels of the NMDA-receptor complex.
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pubmed:language |
rus
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0233-528X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
44
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
64-6
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pubmed:meshHeading | |
pubmed:articleTitle |
[On the mechanism of antimotion sickness effects of mexidol].
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pubmed:publicationType |
Journal Article,
English Abstract
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