期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 56, 期 -, 页码 115-127出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2013.04.006
关键词
Wnt signaling; BDNF; Dendritic spine; Dendrite branching; Synapse
资金
- National Institutes of Health [R01 EY14998]
- Department of Molecular, Cellular, and Developmental Biology
- MRC [MR/J013374/1, G0802241] Funding Source: UKRI
- Medical Research Council [MR/J013374/1, G0802241] Funding Source: researchfish
Dendritic spines are major sites of excitatory synaptic transmission and changes in their numbers and morphology have been associated with neurodevelopmental and neurodegenerative disorders. Brain-derived Neurotrophic Factor (BDNF) is a secreted growth factor that influences hippocampal, striatal and neocortical pyramidal neuron dendritic spine density. However, the mechanisms by which BDNF regulates dendritic spines and how BDNF interacts with other regulators of spines remain unclear. We propose that one mechanism by which BDNF promotes dendritic spine formation is through an interaction with Wnt signaling. Here, we show that Wnt signaling inhibition in cultured cortical neurons disrupts dendritic spine development, reduces dendritic arbor size and complexity, and blocks BDNF-induced dendritic spine formation and maturation. Additionally, we show that BDNF regulates expression of Wnt2, and that Wnt2 is sufficient to promote cortical dendrite growth and dendritic spine formation. Together, these data suggest that BDNF and Wnt Signaling cooperatively regulate dendritic spine formation. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.
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