Neurotrophin and Wnt signaling cooperatively regulate dendritic spine formation.
Neurotrophin and Wnt signaling cooperatively regulate dendritic spine formation.
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DOI：
10.1016/j.mcn.2013.04.006
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发表时间：
2013-09
影响因子：
3.5
通讯作者：
Jones, Kevin R.
中科院分区：
文献类型：
--
作者：
Hiester, Brian G.;Galati, Domenico F.;Salinas, Patricia C.;Jones, Kevin R.
树突棘是兴奋性突触传递的主要部位，其数量和形态的变化与神经发育和神经退行性疾病有关。脑源性神经营养因子(BDNF)是一种分泌型生长因子，可影响海马、纹状体和新皮质锥体神经元树突棘密度。然而，BDNF调节树突棘的机制以及BDNF如何与其他脊椎调节因子相互作用仍不清楚。我们认为BDNF促进树突棘形成的一个机制是通过与Wnt信号的相互作用。在这里，我们发现，在培养的皮质神经元中Wnt信号的抑制扰乱了树突棘的发育，减少了树突棘的大小和复杂性，并阻止了BDNF诱导的树突棘的形成和成熟。此外，我们发现BDNF调节WNT2的表达，WNT2足以促进皮质树突的生长和树突棘的形成。综上所述，这些数据表明BDNF和Wnt信号协同调节树突棘的形成。
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.
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