WAVE1 controls neuronal activity-induced mitochondrial distribution in dendritic spines

Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3112-6. doi: 10.1073/pnas.0712180105. Epub 2008 Feb 14.

Abstract

Mitochondrial fission and trafficking to dendritic protrusions have been implicated in dendritic spine development. Here, we show that Wiskott-Aldrich syndrome protein (WASP)-family verprolin homologous protein 1 (WAVE1) controls depolarization-induced mitochondrial movement into dendritic spines and filopodia and regulates spine morphogenesis. Depolarization-induced degradation of the p35 regulatory subunit of cyclin-dependent kinase 5 (Cdk5), with the resultant decreased inhibitory phosphorylation on WAVE1, depend on NMDA receptor activation. Thus, WAVE1 dephosphorylation and activation are likely associated with mitochondrial redistribution and spine morphogenesis.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dendritic Spines / physiology*
  • Hippocampus / cytology*
  • Image Processing, Computer-Assisted
  • Microscopy, Fluorescence
  • Mitochondria / metabolism
  • Mitochondria / physiology*
  • Phosphorylation
  • RNA Interference
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Wiskott-Aldrich Syndrome Protein Family / metabolism*

Substances

  • Receptors, N-Methyl-D-Aspartate
  • WASF1 protein, human
  • Wiskott-Aldrich Syndrome Protein Family