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The Journal of Neuroscience, December 15, 2001, 21(24):9541-9548
A Role for the Cytoplasmic Polyadenylation Element in NMDA Receptor-Regulated mRNA Translation in Neurons
David G. Wells1, Xin Dong1, Elizabeth M. Quinlan1, Yi-Shuian Huang3, Mark F. Bear1, 2, Joel D. Richter3, and Justin R. Fallon1 1 Department of Neuroscience and 2 Howard Hughes Medical Institute, Brown University, Providence, Rhode Island 02912, and 3 Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655
The ability of neurons to modify synaptic connections based on activity is essential for information processing and storage in the brain. The induction of long-lasting changes in synaptic strength requires new protein synthesis and is often mediated by NMDA-type glutamate receptors (NMDARs). We used a dark-rearing paradigm to examine mRNA translational regulation in the visual cortex after visual experience-induced synaptic plasticity. In this model system, we demonstrate that visual experience induces the translation of mRNA encoding the
-subunit of calcium/calmodulin-dependent kinase II in the visual cortex. Furthermore, this increase in translation is NMDAR dependent. One potential source for newly synthesized proteins is the translational activation of dormant cytoplasmic mRNAs. To examine this possibility, we developed a culture-based assay system to study translational regulation in neurons. Cultured hippocampal neurons were transfected with constructs encoding green fluorescent protein (GFP). At 6 hr after transfection, ~35% of the transfected neurons (as determined by in situ hybridization) expressed detectable GFP protein. Glutamate stimulation of the cultures at this time induced an increase in the number of neurons expressing GFP protein that was NMDAR dependent. Importantly, the glutamate-induced increase was only detected when the 3'-untranslated region of the GFP constructs contained intact cytoplasmic polyadenylation elements (CPEs). Together, these findings define a molecular mechanism for activity-dependent synaptic plasticity that is mediated by the NMDA receptor and requires the CPE-dependent translation of an identified mRNA.
Key words: protein synthesis; synaptic plasticity; CPEB; NMDA receptor; dendrites; visual cortex; hippocampus
Copyright © 2001 Society for Neuroscience 0270-6474/01/21249541-08$05.00/0
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