The Brain-Derived Neurotrophic Factor Enhances Synthesis of Arc in Synaptoneurosomes

Protein synthesis in neurons is essential for the consolidation of memory and for the stabilization of activity-dependent forms of synaptic plasticity such as long-term potentiation (LTP). Activity-dependent translation of dendritically localized mRNAs has been proposed to be a critical source of ne...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2002-02, Vol.99 (4), p.2368-2373
Main Authors: Yin, Yong, Edelman, Gerald M., Vanderklish, Peter W.
Format: Article
Language:English
Subjects:
Animals
Arc protein
Biological Sciences
Biology
Brain
Brain-Derived Neurotrophic Factor - metabolism
Cerebral Cortex - cytology
Cytoskeletal Proteins - biosynthesis
Dendrites - metabolism
Electrophoresis
Hippocampus - cytology
Immunoblotting
Long term potentiation
Memory
Messenger RNA
N methyl D aspartate receptors
Nerve Tissue Proteins - biosynthesis
Neurology
Neurons
Neurons - physiology
Neuroscience
Protein Biosynthesis
Protein synthesis
Proteins
Rats
Rats, Sprague-Dawley
Receptors
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Synapses
Synapses - physiology
Synaptotagmins
Up-Regulation
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Summary:Protein synthesis in neurons is essential for the consolidation of memory and for the stabilization of activity-dependent forms of synaptic plasticity such as long-term potentiation (LTP). Activity-dependent translation of dendritically localized mRNAs has been proposed to be a critical source of new proteins necessary for synaptic change. mRNA for the activity-regulated cytoskeletal protein, Arc, is transcribed during LTP and learning, and disruption of its translation gives rise to deficits in both. We have found that selective translation of Arc in a synaptoneurosomal preparation is induced by the brain-derived neurotrophic factor, a neurotrophin that is released during high-frequency stimulation patterns used to elicit LTP. This effect involves signaling through the TrkB receptor and is blocked by the N-methyl-D-aspartate-type glutamate receptor antagonist, MK801. The results suggest there is a synergy between neurotrophic and ionotropic mechanisms that may influence the specificity and duration of changes in synaptic efficacy at glutamatergic synapses.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.042693699