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pubmed-article:1279482pubmed:abstractTextReceptor binding assays have shown that diaminodecane (DA-10) reduced binding of open channel blockers to the N-methyl-D-aspartate (NMDA) subtype of postsynaptic glutamate receptor through an interaction with the polyamine regulatory site. Because the action of DA-10 was opposite to that of the polyamine agonist spermine and was reversed by polyamine antagonists, DA-10 has been classified as an inverse agonist at the polyamine site. Using whole-cell voltage-clamp and single-channel recordings from cultured rat cortical neurons, we show that at negative holding potentials DA-10 (1-300 microM) reduced NMDA receptor whole cell current (IC50 = 34 microM) and produced a flickery block of NMDA single-channel currents. The flickery block of NMDA single channels was voltage-dependent and not reversed by the polyamine antagonist diethylenetriamine (DET). Potential mechanisms for the flickery block of NMDA single channel currents are discussed.lld:pubmed
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pubmed-article:1279482pubmed:articleTitleThe polyamine diaminodecane (DA-10) produces a voltage-dependent flickery block of single NMDA receptor channels.lld:pubmed
pubmed-article:1279482pubmed:affiliationNeuroscience Program, University of Michigan, Ann Arbor.lld:pubmed
pubmed-article:1279482pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1279482pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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