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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Oligodendrocytes promote neuronal survival and axonal length by distinct intracellular mechanisms: a novel role for oligodendrocyte-derived glial cell line-derived neurotrophic factor.
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Oligodendrocytes promote neuronal survival and axonal length by distinct intracellular mechanisms: a novel role for oligodendrocyte-derived glial cell line-derived neurotrophic factor.

机译：少突胶质细胞通过独特的细胞内机制促进神经元存活和轴突长度：少突胶质细胞衍生的神经胶质细胞系衍生的神经营养因子的新作用。

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摘要

Interactions of CNS cells lead to the establishment of complex neural systems. Specifically, oligodendrocytes form myelin sheaths around axons that enable rapid electrical conduction of impulses. Recent evidence has emerged that oligodendrocytes may also release trophic factors promoting neuronal survival. We therefore studied the effects of factors released from cells of the oligodendrocyte lineage on neuronal survival and also on the morphology of neurons. Neurons derived from rat embryonic cortices were cultured and exposed to media conditioned by oligodendrocyte precursor cells (OPCs) or differentiated oligodendrocytes. In line with previous studies, exposure of OPC and oligodendrocyte-conditioned media (OCM) increased survival, a phosphatidylinositol 3'-kinase (PI3kinase)/Akt-dependent phenomenon. In addition, exposure of neurons to OCM but not OPC conditioned media resulted in increased axonal length per neuron, as detected by antibodies to phosphorylated neurofilaments. OCM exposure resulted in activation of the MAPkinase/extracellular signal-regulated kinase pathway, inhibition of which significantly reduced oligodendrocyte-mediated enhancement of axonal length but, unlike PI3kinase inhibition, had no effect on neuronal survival. Furthermore, we identify glial cell line-derived neurotrophic factor (GDNF) production by differentiated oligodendrocytes and provide evidence that implicates GDNF in OCM-mediated axonal effects, independent of its effect on neuronal survival. Therefore, we have shown that factors released by OPCs and oligodendrocytes induce the activation of distinct intracellular pathways within neurons, which have different functional effects on the cell.
机译：CNS细胞的相互作用导致建立复杂的神经系统。具体而言，少突胶质细胞在轴突周围形成髓鞘，使脉冲能够快速导电。最近的证据表明，少突胶质细胞也可能释放促进神经元存活的营养因子。因此，我们研究了少突胶质细胞系细胞释放的因子对神经元存活以及神经元形态的影响。培养源自大鼠胚胎皮层的神经元，并将其暴露于少突胶质细胞前体细胞（OPC）或分化少突胶质细胞条件下的培养基。与以前的研究一致，OPC和少突胶质细胞条件培养基（OCM）的暴露可提高生存率，这是磷脂酰肌醇3'激酶（PI3激酶）/ Akt依赖性现象。此外，神经元暴露于OCM条件培养基而不是OPC条件培养基会导致每个神经元的轴突长度增加，这可通过磷酸化神经丝抗体来检测。 OCM暴露导致MAP激酶/细胞外信号调节激酶途径的激活，其抑制显着降低了少突胶质细胞介导的轴突长度的增加，但与PI3激酶抑制不同，它对神经元存活没有影响。此外，我们确定了分化的少突胶质细胞产生的胶质细胞源性神经营养因子（GDNF），并提供证据表明GDNF涉及OCM介导的轴突作用，而独立于其对神经元存活的影响。因此，我们已经表明，由OPC和少突胶质细胞释放的因子会诱导神经元内不同的细胞内途径的激活，这对细胞具有不同的功能作用。

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