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在培养的新生浦肯野细胞中,TrkB信号传导可独立于树突结构调节棘突密度和形态。

TrkB signaling modulates spine density and morphology independent of dendrite structure in cultured neonatal Purkinje cells.

作者信息

Shimada A, Mason C A, Morrison M E

机构信息

Departments of Pathology and Anatomy and Cell Biology, Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.

出版信息

J Neurosci. 1998 Nov 1;18(21):8559-70. doi: 10.1523/JNEUROSCI.18-21-08559.1998.

Abstract

Neurotrophins cooperate with neural activity to modulate CNS neuronal survival and dendritic differentiation. In a previous study, we demonstrated that a critical balance of neurotrophin and neural activity is required for Purkinje cell survival in cocultures of purified granule and Purkinje cells (Morrison and Mason, 1998). Here we investigate whether TrkB signaling regulates dendrite and spine development of Purkinje cells. BDNF treatment of purified Purkinje cells cultured alone did not elicit formation of mature dendrites or spines. In cocultures of granule and Purkinje cells, however, continuous treatment with BDNF over a 2 week postnatal culture period increased the density of Purkinje cell dendritic spines relative to controls without causing a shift in the proportions of headed and filopodia-like spines. The increase in spine number was blocked by adding TrkB-IgG to the medium together with BDNF. Although BDNF alone did not consistently modify the morphology of dendritic spines, treatment with TrkB-IgG alone yielded spines with longer necks than those in control cultures. None of these treatments altered Purkinje cell dendritic complexity. These analyses reveal a role for TrkB signaling in modulating spine development, consistent with recently reported effects of neurotrophins on synaptic function. Moreover, spine development can be uncoupled from dendrite outgrowth in this reductionist system of purified presynaptic and postsynaptic neurons.

摘要

神经营养因子与神经活动协同作用,以调节中枢神经系统神经元的存活和树突分化。在先前的一项研究中,我们证明在纯化的颗粒细胞和浦肯野细胞共培养物中,浦肯野细胞的存活需要神经营养因子和神经活动的关键平衡(莫里森和梅森,1998年)。在这里,我们研究TrkB信号是否调节浦肯野细胞的树突和棘突发育。单独培养的纯化浦肯野细胞经脑源性神经营养因子(BDNF)处理后,未引发成熟树突或棘突的形成。然而,在颗粒细胞和浦肯野细胞的共培养物中,在出生后2周的培养期内持续用BDNF处理,相对于对照组,增加了浦肯野细胞树突棘的密度,且未导致有头棘和丝状伪足样棘比例的改变。通过在培养基中加入TrkB-IgG和BDNF,可阻断棘突数量的增加。尽管单独使用BDNF并不能持续改变树突棘的形态,但单独使用TrkB-IgG处理产生的棘突颈部比对照培养物中的更长。这些处理均未改变浦肯野细胞的树突复杂性。这些分析揭示了TrkB信号在调节棘突发育中的作用,这与最近报道的神经营养因子对突触功能的影响一致。此外,在这个纯化的突触前和突触后神经元的简化系统中,棘突发育可以与树突生长解偶联。

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