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Hippocampus. 2016 Jun;26(6):816-31. doi: 10.1002/hipo.22565. Epub 2016 Feb 5.

Nogo-A controls structural plasticity at dendritic spines by rapidly modulating actin dynamics.

Author information

1
Division of Cellular Neurobiology, Zoological Institute, Braunschweig, Germany.
2
Brain Research Institute, University of Zurich, Zurich, Switzerland.
3
Department of Health Sciences and Technology, ETH Zurich, Zurich, Switzerland.
4
Division of Cell Biology, Faculty of Science, Utrecht University Utrecht, Netherlands.
5
Helmholtz Centre for Infection Research, AG NIND, Braunschweig, Germany.

Abstract

Nogo-A and its receptors have been shown to control synaptic plasticity, including negatively regulating long-term potentiation (LTP) in the cortex and hippocampus at a fast time scale and restraining experience-dependent turnover of dendritic spines over days. However, the molecular mechanisms and the precise time course mediating these actions of Nogo-A are largely unexplored. Here we show that Nogo-A signaling in the adult nervous system rapidly modulates the spine actin cytoskeleton within minutes to control structural plasticity at dendritic spines of CA3 pyramidal neurons. Indeed, acute Nogo-A loss-of-function transiently increases F-actin stability and results in an increase in dendritic spine density and length. In addition, Nogo-A acutely restricts AMPAR insertion and mEPSC amplitude at hippocampal synaptic sites. These data indicate a crucial function of Nogo-A in modulating the very tight balance between plasticity and stability of the neuronal circuitry underlying learning processes and the ability to store long-term information in the mature CNS.

KEYWORDS:

AMPA receptor insertion; FRAP; actin cytoskeleton; neurite-growth inhibitors; structural plasticity

PMID:
26748478
DOI:
10.1002/hipo.22565
[Indexed for MEDLINE]

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