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Neuron
Article
License: Elsevier Non-Commercial
Data sources: UnpayWall
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Neuron
Article . 1998
License: Elsevier Non-Commercial
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Neuron
Article . 1998 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
Neuron
Article . 1998
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NSF Binding to GluR2 Regulates Synaptic Transmission

Authors: Nishimune, A; Isaac, JTR; Molnar, E; Noel, JR; Nash, SR; Tagaya, M; Collingridge, GL; +2 Authors

NSF Binding to GluR2 Regulates Synaptic Transmission

Abstract

Here, we show that N-ethylmaleimide-sensitive fusion protein (NSF) interacts directly and selectively with the intracellular C-terminal domain of the GluR2 subunit of AMPA receptors. The interaction requires all three domains of NSF but occurs between residues Lys-844 and Gln-853 of rat GluR2, with Asn-851 playing a critical role. Loading of decapeptides corresponding to the NSF-binding domain of GluR2 into rat hippocampal CA1 pyramidal neurons results in a marked, progressive decrement of AMPA receptor-mediated synaptic transmission. This reduction in synaptic transmission was also observed when an anti-NSF monoclonal antibody (mAb) was loaded into CA1 neurons. These results demonstrate a previously unsuspected direct interaction in the postsynaptic neuron between two major proteins involved in synaptic transmission and suggest a rapid NSF-dependent modulation of AMPA receptor function.

Country
United Kingdom
Keywords

Neurons, Neuroscience(all), Molecular Sequence Data, Vesicular Transport Proteins, Antibodies, Monoclonal, Excitatory Postsynaptic Potentials, Hippocampus, Synaptic Transmission, Rats, Receptors, Glutamate, Excitatory Amino Acid Agonists, Animals, Amino Acid Sequence, Receptors, AMPA, Rats, Wistar, Carrier Proteins, N-Ethylmaleimide-Sensitive Proteins, alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid, Cells, Cultured

  • BIP!
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    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    489
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 1%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 1%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 0.1%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
489
Top 1%
Top 1%
Top 0.1%
hybrid