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  Miniature neurotransmission stabilizes synaptic function via tonic suppression of local dendritic protein synthesis

Sutton, M. A., Ito, H., Cressy, P., Kempf, C., Woo, J. C., & Schuman, E. M. (2006). Miniature neurotransmission stabilizes synaptic function via tonic suppression of local dendritic protein synthesis. Cell, 125(4), 785-799. doi:10.1016/j.cell.2006.03.040.

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Sutton, M. A., Author
Ito, Hiroshi1, Author              
Cressy, P., Author
Kempf, C., Author
Woo, J. C., Author
Schuman, E. M., Author
Affiliations:
1Memory and Navigation Circuits Group, Max Planck Institute for Brain Research, Max Planck Society, ou_2461699              

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Free keywords: Action Potentials/physiology Animals Cells, Cultured Cobalt/metabolism Dendrites/*metabolism Excitatory Amino Acid Agonists/metabolism Excitatory Postsynaptic Potentials/*physiology Hippocampus/cytology/metabolism Homeostasis In Vitro Techniques Nerve Tissue Proteins/*biosynthesis Patch-Clamp Techniques Protein Subunits/metabolism Rats Receptors, AMPA/metabolism Receptors, N-Methyl-D-Aspartate/metabolism Signal Transduction/physiology Synapses/*physiology Synaptic Transmission/*physiology
 Abstract: Activity deprivation in neurons induces a slow compensatory scaling up of synaptic strength, reflecting a homeostatic mechanism for stabilizing neuronal activity. Prior studies have focused on the loss of action potential (AP) driven neurotransmission in synaptic homeostasis. Here, we show that the miniature synaptic transmission that persists during AP blockade profoundly shapes the time course and mechanism of homeostatic scaling. A brief blockade of NMDA receptor (NMDAR) mediated miniature synaptic events ("minis") rapidly scales up synaptic strength, over an order of magnitude faster than with AP blockade alone. The rapid scaling induced by NMDAR mini blockade is mediated by increased synaptic expression of surface GluR1 and the transient incorporation of Ca2+-permeable AMPA receptors at synapses; both of these changes are implemented locally within dendrites and require dendritic protein synthesis. These results indicate that NMDAR signaling during miniature synaptic transmission serves to stabilize synaptic function through active suppression of dendritic protein synthesis.

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 Dates: 2006
 Publication Status: Published in print
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 Rev. Type: -
 Identifiers: Other: 16713568
DOI: 10.1016/j.cell.2006.03.040
ISSN: 0092-8674 (Print)0092-8674 (Linking)
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Title: Cell
Source Genre: Journal
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Pages: - Volume / Issue: 125 (4) Sequence Number: - Start / End Page: 785 - 799 Identifier: -