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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Groth, Rachel D. Thiagarajan, Tara C. Li, Li Tsien, Richard W. Lindskog, Maria |
| Description | Author Affiliation: Groth RD ( Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA.); |
| Abstract | Prolonged AMPA-receptor blockade in hippocampal neuron cultures leads to both an increased expression of GluA1 postsynaptically and an increase in vesicle pool size and turnover rate presynaptically, adaptive changes that extend beyond simple synaptic scaling. As a molecular correlate, expression of the ß Ca(2+)/CaM-dependent kinase type II (ßCaMKII) is increased in response to synaptic inactivity. Here we set out to clarify the role of ßCaMKII in the various manifestations of adaptation. Knockdown of ßCaMKII by lentiviral-mediated expression of shRNA prevented the synaptic inactivity-induced increase in GluA1, as did treatment with the CaM kinase inhibitor KN-93, but not the inactive analog KN-92. These results demonstrate that, spurred by AMPA-receptor blockade, up-regulation of ßCaMKII promotes increased GluA1 expression. Indeed, transfection of ßCaMKII, but not a kinase-dead mutant, increased GluA1 expression on dendrites and elevated vesicle turnover (Syt-Ab uptake), mimicking the effect of synaptic inactivity on both sides of the synapse. In cells with elevated ßCaMKII, relief of synaptic-activity blockade uncovered an increase in the frequency of miniature excitatory postsynaptic currents that could be rapidly and fully suppressed by PhTx blockade of GluA1 receptors. This increased mini frequency involved a genuine presynaptic enhancement, not merely an increased abundance of synapses. This finding suggests that Ca(2+) flux through GluA1 receptors may trigger the acute release of a retrograde messenger. Taken together, our results indicate that synaptic inactivity-induced increases in ßCaMKII expression set in motion a series of events that culminate in coordinated pre- and postsynaptic adaptations in synaptic transmission. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 2 |
| Volume Number | 108 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2011-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Calcium-Calmodulin-Dependent Protein Kinase Type 2 Metabolism Hippocampus Neurons Receptors, AMPA Synaptic Transmission Animals Benzylamines Pharmacology Green Fluorescent Proteins Homeostasis Lentivirus Genetics Mice Microscopy, Fluorescence Protein Kinase Inhibitors RNA, Small Interfering Signal Transduction Sulfonamides Up-Regulation Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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