WIP is a negative regulator of neuronal maturation and synaptic activity

A. Franco, S. Knafo, I. Banon-Rodriguez, P. Merino-Serrais, I. Fernaud-Espinosa, M. Nieto, J. J. Garrido, J. A. Esteban, F. Wandosell, I. M. Anton

Research output: Contribution to journalArticlepeer-review

Abstract

Wiskott-Aldrich syndrome protein (WASP)-interacting protein (WIP) is an actin-binding protein involved in the regulation of actin polymerization in cells, such as fibroblasts and lymphocytes. Despite its recognized function in non-neuronal cells, the role of WIP in the central nervous system has not been examined previously. We used WIP-deficient mice to examine WIP function both in vivo and in vitro. We report here that WIP -/- hippocampal neurons exhibit enlargement of somas as well as overgrowth of neuritic and dendritic branches that are more evident in early developmental stages. Dendritic arborization and synaptogenesis, which includes generation of postsynaptic dendritic spines, are actin-dependent processes that occur in parallel at later stages. WIP deficiency also increases the amplitude and frequency of miniature excitatory postsynaptic currents, suggesting that WIP -/- neurons have more mature synapses than wild-type neurons. These findings reveal WIP as a previously unreported regulator of neuronal maturation and synaptic activity.

Original languageAmerican English
Pages (from-to)1191-1202
Number of pages12
JournalCerebral Cortex
Volume22
Issue number5
DOIs
StatePublished - 1 May 2012
Externally publishedYes

Keywords

  • N-WASP
  • dendritic spine
  • electrophysiology
  • neuritogenesis
  • synapse

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cognitive Neuroscience

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