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

Neuron | Jul 3, 2002

http://www.ncbi.nlm.nih.gov/pubmed/12123613

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 RIS Download

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

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