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首页> 外文期刊>The European Journal of Neuroscience >Olfactory bulb hypoplasia in Prokr2 null mice stems from defective neuronal progenitor migration and differentiation.
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Olfactory bulb hypoplasia in Prokr2 null mice stems from defective neuronal progenitor migration and differentiation.

机译:Prokr2 null小鼠的嗅球发育不全源于有缺陷的神经元祖细胞迁移和分化。

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摘要

New neurons are added on a daily basis to the olfactory bulb (OB) of a mammal, and this phenomenon exists throughout its lifetime. These new cells are born in the subventricular zone and migrate to the OB via the rostral migratory stream (RMS). To examine the role of the prokineticin receptor 2 (Prokr2) in neurogenesis, we created a Prokr2 null mouse, and report a decrease in the volume of its OB and also a decrease in the number of bromodeoxyuridine (BrdU)-positive cells. There is disrupted architecture of the OB, with the glomerular layer containing terminal dUTP nick-end labeling (TUNEL) -positive nuclei and also a decrease in tyrosine hydroxylase-positive neurons in this layer. In addition, there are increased numbers of doublecortin-positive neuroblasts in the RMS and increased PSA-NCAM (polysialylated form of the neural cell adhesion molecule) -positive neuronal progenitors around the olfactory ventricle, indicating their detachment from homotypic chains is compromised. Finally, in support of this, Prokr2-deficient cells expanded in vitro as neurospheres are incapable of migrating towards a source of recombinant human prokineticin 2 (PROK2). Together, these findings suggest an important role for Prokr2 in OB neurogenesis.
机译:每天都会向哺乳动物的嗅球(OB)添加新的神经元,并且这种现象在其整个生命周期中都存在。这些新细胞出生在脑室下区,并通过鼻迁移流(RMS)迁移至OB。为了检查促动素受体2(Prokr2)在神经发生中的作用,我们创建了一个Prokr2 null小鼠,并报告了其OB体积的减少以及溴脱氧尿苷(BrdU)阳性细胞的数量的减少。 OB的结构受到破坏,肾小球层包含末端dUTP缺口末端标记(TUNEL)阳性核,并且该层中酪氨酸羟化酶阳性神经元减少。另外,RMS中的双皮质素阳性神经母细胞数目增加,并且嗅觉心室周围的PSA-NCAM(神经细胞粘附分子的多唾液酸化形式)阳性神经元祖细胞增加,表明它们与同型链的分离受到损害。最后,为此提供支持的Prokr2缺陷细胞在体外扩增,因为神经球无法迁移至重组人促动蛋白2(PROK2)的来源。在一起,这些发现表明Prokr2在OB神经发生中的重要作用。

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