Abstract
Phosphatase IIb (calcineurin, CaN) can reduce N-methyl-D-aspartate (NMDA) synaptic responses by enhancing glycine-independent desensitization. We examined the action of CaN on desensitization in recombinant NMDA receptors comprised of NMDA receptor 1 (NR1) and NR2A subunits. The C-terminus of NR2A, but not NR1, was critical for modulation of desensitization by CaN. Alanine-scanning mutagenesis indicated that serines 900 and 929 in NR2A altered desensitization, as did inhibition of tyrosine phosphatases. Our data suggest that dephosphorylation-dependent regulation of the C-terminus of NR2A increases desensitization of NMDA receptors, providing an additional mechanism for modulation of synaptic signals.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Calcineurin / metabolism
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Calcineurin Inhibitors*
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Cell Line
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Enzyme Inhibitors / pharmacology
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Glycine / physiology
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Humans
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Mutation / physiology
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Organometallic Compounds / pharmacology
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Phenanthrolines / pharmacology
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Protein Tyrosine Phosphatases / antagonists & inhibitors
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Receptors, N-Methyl-D-Aspartate / chemistry
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Receptors, N-Methyl-D-Aspartate / genetics
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Receptors, N-Methyl-D-Aspartate / physiology*
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Recombinant Proteins / metabolism
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Serine / genetics
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Vanadium / pharmacology
Substances
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Calcineurin Inhibitors
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Enzyme Inhibitors
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NMDA receptor A1
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NR2A NMDA receptor
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Organometallic Compounds
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Phenanthrolines
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Receptors, N-Methyl-D-Aspartate
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Recombinant Proteins
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Vanadium
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Serine
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bisperoxo(1,10-phenanthroline)oxovanadate(1-)
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Calcineurin
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Protein Tyrosine Phosphatases
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Glycine