期刊
JOURNAL OF NEUROSCIENCE
卷 31, 期 35, 页码 12426-12436出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0685-11.2011
关键词
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资金
- Recombinant Protein Biochemistry Core [P30 EY020799]
- NIDA [T32DA07290]
- University of Texas Southwestern Medical Center
- Whitehall Foundation
- National Eye Institute [R01 EY018207]
- National Institute on Drug Abuse [P01 DA008277]
Brain-derived neurotrophic factor (BDNF) and its cognate receptor, TrkB, regulate a wide range of cellular processes, including dendritic spine formation and functional synapse plasticity. However, the signaling mechanisms that link BDNF-activated TrkB to F-actin remodeling enzymes and dendritic spine morphological plasticity remain poorly understood. We report here that BDNF/TrkB signaling in neurons activates the Vav family of Rac/RhoA guanine nucleotide exchange factors through a novel TrkB-dependent mechanism. We find that Vav is required for BDNF-stimulated Rac-GTP production in cortical and hippocampal neurons. Vav is partially enriched at excitatory synapses in the postnatal hippocampus but does not appear to be required for normal dendritic spine density. Rather, we observe significant reductions in both BDNF-induced, rapid, dendritic spine head growth and in CA3-CA1 theta burst-stimulated long-term potentiation in Vav-deficient mouse hippocampal slices, suggesting that Vav-dependent regulation of dendritic spine morphological plasticity facilitates normal functional synapse plasticity.
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