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

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.

Pubmed ID: 12123613

Authors

  • Meng Y
  • Zhang Y
  • Tregoubov V
  • Janus C
  • Cruz L
  • Jackson M
  • Lu WY
  • MacDonald JF
  • Wang JY
  • Falls DL
  • Jia Z

Journal

Neuron

Publication Data

July 3, 2002

Associated Grants

None

Mesh Terms

  • Actin Cytoskeleton
  • Actin Depolymerizing Factors
  • Animals
  • Cell Differentiation
  • Cells, Cultured
  • Conditioning (Psychology)
  • Cytoskeleton
  • DNA-Binding Proteins
  • Dendrites
  • Excitatory Postsynaptic Potentials
  • Fear
  • Female
  • Hippocampus
  • Lim Kinases
  • Long-Term Potentiation
  • Male
  • Maze Learning
  • Mice
  • Mice, Knockout
  • Microfilament Proteins
  • Microtubule-Associated Proteins
  • Motor Activity
  • Mutation
  • Nervous System Malformations
  • Neural Inhibition
  • Protein Kinases
  • Protein-Serine-Threonine Kinases
  • Up-Regulation
  • Williams Syndrome