RGD Reference Report - Kalirin-7 controls activity-dependent structural and functional plasticity of dendritic spines. - Rat Genome Database

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Kalirin-7 controls activity-dependent structural and functional plasticity of dendritic spines.

Authors: Xie, Zhong  Srivastava, Deepak P  Photowala, Huzefa  Kai, Li  Cahill, Michael E  Woolfrey, Kevin M  Shum, Cassandra Y  Surmeier, D James  Penzes, Peter 
Citation: Xie Z, etal., Neuron. 2007 Nov 21;56(4):640-56.
RGD ID: 12050112
Pubmed: (View Article at PubMed) PMID:18031682
DOI: Full-text: DOI:10.1016/j.neuron.2007.10.005

Activity-dependent rapid structural and functional modifications of central excitatory synapses contribute to synapse maturation, experience-dependent plasticity, and learning and memory and are associated with neurodevelopmental and psychiatric disorders. However, the signal transduction mechanisms that link glutamate receptor activation to intracellular effectors that accomplish structural and functional plasticity are not well understood. Here we report that NMDA receptor activation in pyramidal neurons causes CaMKII-dependent phosphorylation of the guanine-nucleotide exchange factor (GEF) kalirin-7 at residue threonine 95, regulating its GEF activity, leading to activation of small GTPase Rac1 and rapid enlargement of existing spines. Kalirin-7 also interacts with AMPA receptors and controls their synaptic expression. By demonstrating that kalirin expression and spine localization are required for activity-dependent spine enlargement and enhancement of AMPAR-mediated synaptic transmission, our study identifies a signaling pathway that controls structural and functional spine plasticity.

Annotation

Objects Annotated

Genes (Rattus norvegicus)
Kalrn  (kalirin, RhoGEF kinase)


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