BDNF-Dependent Recycling Facilitates TrkB Translocation to Postsynaptic Density during LTP via a Rab11-Dependent Pathway

Autor: Jing Yan, Zhao Geng, Bing Chen, Shuhong Huang, Jue Wang, Zhe-Yu Chen, Wen-Hai Sui, Xiao-Yan Zhang
Rok vydání: 2013
Předmět:
Male
Patch-Clamp Techniques
Long-Term Potentiation
Endocytic recycling
Tropomyosin receptor kinase B
In Vitro Techniques
Tropomyosin receptor kinase A
Biology
Hippocampus
Rats
Sprague-Dawley
Synapse
Neurotrophic factors
In Situ Nick-End Labeling
Animals
Immunoprecipitation
Receptor
trkB
Biotinylation
Neurons
Analysis of Variance
Brain-Derived Neurotrophic Factor
musculoskeletal
neural
and ocular physiology
General Neuroscience
Intracellular Signaling Peptides and Proteins
Membrane Proteins
Post-Synaptic Density
Long-term potentiation
Articles
Embryo
Mammalian
Electric Stimulation
Rats
Cell biology
Protein Transport
Animals
Newborn
nervous system
rab GTP-Binding Proteins
embryonic structures
Synaptic plasticity
Female
Disks Large Homolog 4 Protein
Neuroscience
Postsynaptic density
Protein Binding
Subcellular Fractions
Zdroj: The Journal of Neuroscience. 33:9214-9230
ISSN: 1529-2401
0270-6474
Popis: Brain-derived neurotrophic factor (BDNF) plays an important role in the activity-dependent regulation of synaptic structure and function via tropomyosin related kinase B (TrkB) receptor activation. However, whether BDNF could regulate TrkB levels at synapse during long-term potentiation (LTP) is still unknown. We show in cultured rat hippocampal neurons that chemical LTP (cLTP) stimuli selectively promote endocytic recycling of BDNF-dependent full-length TrkB (TrkB-FL) receptors, but not isoform T1 (TrkB.T1) receptors, via a Rab11-dependent pathway. Moreover, neuronal-activity-enhanced TrkB-FL recycling could facilitate receptor translocation to postsynaptic density and enhance BDNF-induced extracellular signal-regulated kinase and phosphatidylinositol 3-kinase activation and rat hippocampal neuron survival. Finally, we found that cLTP could stimulate the switch of Rab11 from an inactive to an active form and that GTP-bound Rab11 could enhance the interaction between TrkB-FL and PSD-95. Therefore, the recycling endosome could serve as a reserve pool to supply TrkB-FL receptors for LTP maintenance. These findings provide a mechanistic link between Rab11-dependent endocytic recycling and TrkB modulation of synaptic plasticity.
Databáze: OpenAIRE
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