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Scribble1/AP2 complex coordinates NMDA receptor endocytic recycling.

Nicolas H Piguel1, Sabine Fievre2, Jean-Michel Blanc3

  • 1Physiopathologie de la Plasticité Neuronale, Neurocentre Magendie, INSERM, U862, 33000 Bordeaux, France; Neurocentre Magendie, University of Bordeaux, U862, 33000 Bordeaux, France.

Cell Reports
|October 15, 2014
PubMed
Summary
This summary is machine-generated.

Scribble1 protein levels change with neural activity and regulate the number of NMDA receptors (NMDARs) at synapses. Scribble1 promotes NMDAR recycling, preventing their degradation and maintaining synaptic plasticity.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Glutamate receptor trafficking is essential for synaptic function and plasticity.
  • NMDA receptors (NMDARs) dynamically exchange between synaptic and extrasynaptic pools, influencing synaptic plasticity.
  • Scribble1, a PDZ protein, is critical for synaptogenesis and synaptic plasticity.

Purpose of the Study:

  • To investigate the role of Scribble1 in regulating NMDA receptor (NMDAR) levels at synapses.
  • To elucidate the molecular mechanisms by which Scribble1 controls NMDAR trafficking and synaptic plasticity.

Main Methods:

  • Activity-dependent regulation of Scribble1 levels was assessed.
  • The impact of Scribble1 on NMDAR surface expression was quantified.
  • Mechanisms of NMDAR recycling and degradation were investigated.
  • Protein-protein interactions involving Scribble1 and AP2 were analyzed.

Main Results:

  • Scribble1 levels are regulated in an activity-dependent manner.
  • Scribble1 controls the number of NMDARs at the plasma membrane.
  • Scribble1 inhibits lysosomal trafficking and degradation of GluN2A subunits by promoting NMDAR recycling.
  • A YxxR motif in Scribble1 mediates interaction with AP2, controlling these processes.

Conclusions:

  • Scribble1 acts as a key regulator of synaptic NMDAR levels.
  • Activity-dependent regulation of Scribble1 influences NMDAR trafficking and synaptic plasticity.
  • The Scribble1-AP2 interaction defines a novel mechanism for controlling synaptic NMDAR homeostasis.