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首页> 外文期刊>Journal of neuroendocrinology >Calorie restriction activates new adult born olfactory‐bulb neurones in a ghrelin‐dependent manner but acyl‐ghrelin does not enhance subventricular zone neurogenesis
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Calorie restriction activates new adult born olfactory‐bulb neurones in a ghrelin‐dependent manner but acyl‐ghrelin does not enhance subventricular zone neurogenesis

机译：卡路里限制在依赖Ghrelin依赖性的方式中激活新的成人出生的嗅疱泡神经元，但酰基-Ghrelin不会增强脑室区域神经发生

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Abstract The ageing and degenerating brain show deficits in neural stem/progenitor cell ( NSPC ) plasticity that are accompanied by impairments in olfactory discrimination. Emerging evidence suggests that the gut hormone ghrelin plays an important role in protecting neurones, promoting synaptic plasticity and increasing hippocampal neurogenesis in the adult brain. In the present study, we investigated the role of ghrelin with respect to modulating adult subventricular zone ( SVZ ) NSPC s that give rise to new olfactory bulb ( OB ) neurones. We characterised the expression of the ghrelin receptor, growth hormone secretagogue receptor ( GHSR ), using an immunohistochemical approach in GHSR ‐ eGFP reporter mice to show that GHSR is expressed in several regions, including the OB but not in the SVZ of the lateral ventricle. These data suggest that acyl‐ghrelin does not mediate a direct effect on NSPC in the SVZ . Consistent with these findings, treatment with acyl‐ghrelin or genetic silencing of GHSR did not alter NSPC proliferation within the SVZ . Similarly, using a bromodeoxyuridine pulse‐chase approach, we show that peripheral treatment of adult rats with acyl‐ghrelin did not increase the number of new adult‐born neurones in the granule cell layer of the OB . These data demonstrate that acyl‐ghrelin does not increase adult OB neurogenesis. Finally, we investigated whether elevating ghrelin indirectly, via calorie restriction ( CR ), regulated the activity of new adult‐born cells in the OB . Overnight CR induced c‐Fos expression in new adult‐born OB cells but not in developmentally born cells, whereas neuronal activity was absent following re‐feeding. These effects were not present in ghrelin ?/? mice, suggesting that adult‐born cells are uniquely sensitive to changes in ghrelin mediated by fasting and re‐feeding. In summary, ghrelin does not promote neurogenesis in the SVZ and OB ; however, new adult‐born OB cells are activated by CR in a ghrelin‐dependent manner.
机译：摘要衰老和退化性脑在神经茎/祖细胞（NSPC）可塑性中的缺陷伴随着嗅觉歧视的损伤。新兴的证据表明，肠道激素Ghrelin在保护神经元中发挥着重要作用，促进突触可塑性和增加成年大脑的海马神经发生。在本研究中，我们研究了Ghrelin对调节成人脑内区（SVZ）NSPC S产生新的嗅灯泡（OB）神经元的作用。我们以GHSR - EGFP报告小鼠的免疫组织化学方法表明Ghrelin受体，生长激素催化剂受体（GHSR）的表达表明GHSR在几个区域中表达，包括OB但不在侧脑室的SVZ中。这些数据表明acyl-ghrelin不会在SVZ中对NSPC进行直接影响。与这些发现一致，用酰基-Ghrelin或GHSR的遗传沉默治疗没有改变SVZ内的NSPC增殖。类似地，使用溴肟脲脉冲序列方法，我们表明，酰基Ghrelin的成年大鼠的外周治疗没有增加OB颗粒细胞层中的新成人神经元的数量。这些数据表明acyl-ghrelin不会增加成人ob神经发生。最后，我们研究了通过卡路里限制（CR）间接升高Ghrelin，调节OB中新成人出生的细胞的活动。过夜Cr诱导新成人出生的OB细胞中的C-FOS表达，但不在发育出生的细胞中，而重新喂养后神经元活性不存在。 Ghrelin中不存在这些效果？/？小鼠，表明成人出生的细胞对通过禁食和再喂养介导的Ghrelin的变化是唯一敏感的。总之，Ghrelin不会在SVZ和OB中促进神经发生;然而，新的成人出生的OB细胞通过CR以Ghrelin依赖的方式激活。

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