Abnormal spine morphology and enhanced LTP in LIMK-1 knockout mice

Neuron. 2002 Jul 3;35(1):121-33. doi: 10.1016/s0896-6273(02)00758-4.

Abstract

In vitro studies indicate a role for the LIM kinase family in the regulation of cofilin phosphorylation and actin dynamics. In addition, abnormal expression of LIMK-1 is associated with Williams syndrome, a mental disorder with profound deficits in visuospatial cognition. However, the in vivo function of this family of kinases remains elusive. Using LIMK-1 knockout mice, we demonstrate a significant role for LIMK-1 in vivo in regulating cofilin and the actin cytoskeleton. Furthermore, we show that the knockout mice exhibited significant abnormalities in spine morphology and in synaptic function, including enhanced hippocampal long-term potentiation. The knockout mice also showed altered fear responses and spatial learning. These results indicate that LIMK-1 plays a critical role in dendritic spine morphogenesis and brain function.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Actin Cytoskeleton / metabolism*
  • Actin Cytoskeleton / ultrastructure
  • Actin Depolymerizing Factors
  • Animals
  • Cell Differentiation / genetics*
  • Cells, Cultured
  • Conditioning, Psychological / physiology
  • Cytoskeleton / metabolism
  • Cytoskeleton / pathology
  • Cytoskeleton / ultrastructure
  • DNA-Binding Proteins / deficiency*
  • DNA-Binding Proteins / genetics
  • Dendrites / metabolism
  • Dendrites / pathology*
  • Dendrites / ultrastructure
  • Excitatory Postsynaptic Potentials / genetics
  • Fear / physiology
  • Female
  • Hippocampus / abnormalities*
  • Hippocampus / growth & development
  • Hippocampus / pathology
  • Lim Kinases
  • Long-Term Potentiation / genetics*
  • Male
  • Maze Learning / physiology
  • Mice
  • Mice, Knockout
  • Microfilament Proteins / metabolism*
  • Microtubule-Associated Proteins / metabolism
  • Motor Activity / genetics
  • Mutation / physiology
  • Nervous System Malformations / genetics
  • Nervous System Malformations / metabolism
  • Nervous System Malformations / pathology
  • Neural Inhibition / genetics
  • Protein Kinases
  • Protein Serine-Threonine Kinases / deficiency*
  • Protein Serine-Threonine Kinases / genetics
  • Up-Regulation / genetics
  • Williams Syndrome / genetics
  • Williams Syndrome / metabolism
  • Williams Syndrome / pathology

Substances

  • Actin Depolymerizing Factors
  • DNA-Binding Proteins
  • Microfilament Proteins
  • Microtubule-Associated Proteins
  • Protein Kinases
  • Lim Kinases
  • Limk1 protein, mouse
  • Protein Serine-Threonine Kinases