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

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

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. © 2016 Wiley Periodicals, Inc.

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

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Animals
  • CA3 Region, Hippocampal / metabolism
  • Cells, Cultured
  • Dendritic Spines / metabolism*
  • Excitatory Postsynaptic Potentials / physiology
  • Mice, Inbred C57BL
  • Miniature Postsynaptic Potentials / physiology
  • Neuronal Plasticity / physiology
  • Nogo Proteins / metabolism*
  • Pyramidal Cells / physiology
  • Rats, Wistar
  • Receptors, AMPA / metabolism
  • Tissue Culture Techniques

Substances

  • Actins
  • Nogo Proteins
  • Receptors, AMPA
  • Rtn4 protein, mouse
  • Rtn4 protein, rat