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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Tatavarty, Vedakumar Lin, Heather Turrigiano, Gina G. Gainey, Melanie A. Nahmani, Marc |
| Description | Author Affiliation: Gainey MA ( Department of Biology and Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454.); Tatavarty V ( Department of Biology and Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454.); Nahmani M ( Department of Biology and Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454.); Lin H ( Department of Biology and Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454.); Turrigiano GG ( Department of Biology and Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454 turrigiano@brandeis.edu.); |
| Abstract | Synaptic scaling is a form of homeostatic plasticity that stabilizes neuronal firing in response to changes in synapse number and strength. Scaling up in response to action-potential blockade is accomplished through increased synaptic accumulation of GluA2-containing AMPA receptors (AMPAR), but the receptor trafficking steps that drive this process remain largely obscure. Here, we show that the AMPAR-binding protein glutamate receptor-interacting protein-1 (GRIP1) is essential for regulated synaptic AMPAR accumulation during scaling up. Synaptic abundance of GRIP1 was enhanced by activity deprivation, directly increasing synaptic GRIP1 abundance through overexpression increased the amplitude of AMPA miniature excitatory postsynaptic currents (mEPSCs), and shRNA-mediated GRIP1 knockdown prevented scaling up of AMPA mEPSCs. Furthermore, knockdown and replace experiments targeting either GRIP1 or GluA2 revealed that scaling up requires the interaction between GRIP1 and GluA2. Finally, GRIP1 synaptic accumulation during scaling up did not require GluA2 binding. Taken together, our data support a model in which activity-dependent trafficking of GRIP1 to synaptic sites drives the forward trafficking and enhanced synaptic accumulation of GluA2-containing AMPAR during synaptic scaling up. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 27 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-07-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Action Potentials Physiology Carrier Proteins Metabolism Nerve Tissue Proteins Neurons Synapses Drug Effects Genetics Animals Animals, Newborn Cells, Cultured Excitatory Postsynaptic Potentials Microscopy, Confocal Microscopy, Immunoelectron Ultrastructure Patch-Clamp Techniques Protein Binding RNA Interference Rats, Long-Evans Receptors, AMPA Tetrodotoxin Pharmacology Research Support, N.I.H., Extramural Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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