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首页> 外文期刊>The European Journal of Neuroscience >IGF-I promotes neuronal migration and positioning in the olfactory bulb and the exit of neuroblasts from the subventricular zone.
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IGF-I promotes neuronal migration and positioning in the olfactory bulb and the exit of neuroblasts from the subventricular zone.

机译：IGF-I促进神经元在嗅球中的迁移和定位以及成神经细胞从脑室下区域的出口。

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While insulin-like growth factor-I (IGF-I) supports neuronal and glial differentiation in the CNS, it is largely unknown whether IGF-I also influences neuronal migration and positioning. We show here that the pattern of olfactory bulb (OB) layering is altered in Igf-I (-/-) mice. In these animals, Tbr1(+)-glutamatergic neurons are misplaced in the mitral cell layer (ML) and the external plexiform layer (EPL). In addition, there are fewer interneurons in the glomerular layer and the EPL of the Igf-I (-/-) mice, and fewer newborn neurons are incorporated into the OB from the forebrain subventricular zone (SVZ). Indeed, neuroblasts accumulate in the postnatal/adult SVZ of Igf-I (-/-) mice. Significantly, the positioning of Tbr1(+)-cells in a primitive ML is stimulated by IGF-I in cultured embryonic OB slices, an effect that is partially repressed by the phosphoinositide 3-kinase (PI3K) inhibitor. In OB cell cultures, IGF-I increases the phosphorylation of disabled1 (P-Dab1), an adaptor protein that is a target of Src family kinases (SFK) in the reelin signalling pathway, whereas reduced P-Dab1 levels were found in Igf-I (-/-) mice. Neuroblast migration from the rostral migratory stream (RMS) explants of postnatal Igf-I (-/-) was similar to that from Igf-I (+/+) explants. However, cell migration was significantly enhanced by IGF-I added to the explants, an effect that was repressed by PI3K and SFK inhibitors. These findings suggest that IGF-I promotes neuronal positioning in the OB and support a role for IGF-I in stimulating neuroblast exit from the SVZ into the RMS, thereby promoting the incorporation of newly formed neurons into the OB.
机译：虽然胰岛素样生长因子-I（IGF-I）支持中枢神经系统中神经元和神经胶质的分化，但很大程度上尚不清楚IGF-I是否也会影响神经元的迁移和定位。我们在这里显示，在Igf-I（-/-）小鼠中嗅球（OB）分层的模式已改变。在这些动物中，Tbr1（+）-谷氨酸能神经元放错在二尖瓣细胞层（ML）和外部丛状层（EPL）中。此外，Igf-I（-/-）小鼠的肾小球层和EPL中的中间神经元更少，并且从前脑室下区（SVZ）进入OB的新生神经元也更少。实际上，成神经细胞在Igf-I（-/-）小鼠的出生后/成人SVZ中积累。重要的是，在培养的胚胎OB切片中，IGF-I刺激了原始ML中Tbr1（+）-细胞的定位，而磷酸肌醇3-激酶（PI3K）抑制剂部分抑制了这种作用。在OB细胞培养物中，IGF-I增加了disable1（P-Dab1）的磷酸化，disdis1是在reelin信号通路中作为Src家族激酶（SFK）靶标的衔接蛋白，而在Igf-中发现降低的P-Dab1水平。我（-/-）老鼠。产后Igf-I（-/-）的延性迁徙（RMS）外植体的成神经细胞迁移与Igf-I（+ / +）外植体的成神经细胞迁移相似。但是，通过将IGF-I添加到外植体中，可以显着增强细胞迁移，而PI3K和SFK抑制剂则抑制了这种作用。这些发现表明，IGF-I促进了OB中神经元的定位，并支持了IGF-I在刺激成神经细胞从SVZ离开进入RMS中的作用，从而促进了新形成的神经元向OB的结合。

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