Hillje Anna-Lena, Beckmann Elisabeth, Pavlou Maria A S, Jaeger Christian, Pacheco Maria P, Sauter Thomas, Schwamborn Jens C, Lewejohann Lars
ZMBE, Institute of Cell Biology, Stem Cell Biology and Regeneration Group, Westfälische Wilhelms-Universität Münster Münster, Germany ; Luxembourg Centre for Systems Biomedicine, University of Luxembourg Luxembourg, Luxembourg.
Department of Behavioural Biology, Westfälische Wilhelms-Universität Münster Münster, Germany.
Front Cell Neurosci. 2015 Mar 18;9:75. doi: 10.3389/fncel.2015.00075. eCollection 2015.
In mammals, new neurons are generated throughout the entire lifespan in two restricted areas of the brain, the dentate gyrus (DG) of the hippocampus and the subventricular zone (SVZ)-olfactory bulb (OB) system. In both regions newborn neurons display unique properties that clearly distinguish them from mature neurons. Enhanced excitability and increased synaptic plasticity enables them to add specific properties to information processing by modulating the existing local circuitry of already established mature neurons. Hippocampal neurogenesis has been suggested to play a role in spatial-navigation learning, spatial memory, and spatial pattern separation. Cumulative evidences implicate that adult-born OB neurons contribute to learning processes and odor memory. We recently demonstrated that the cell fate determinant TRIM32 is upregulated in differentiating neuroblasts of the SVZ-OB system in the adult mouse brain. The absence of TRIM32 leads to increased progenitor cell proliferation and less cell death. Both effects accumulate in an overproduction of adult-generated OB neurons. Here, we present novel data from behavioral studies showing that such an enhancement of OB neurogenesis not necessarily leads to increased olfactory performance but in contrast even results in impaired olfactory capabilities. In addition, we show at the cellular level that TRIM32 protein levels increase during differentiation of neural stem cells (NSCs). At the molecular level, several metabolic intermediates that are connected to glycolysis, glycine, or cysteine metabolism are deregulated in TRIM32 knockout mice brain tissue. These metabolomics pathways are directly or indirectly linked to anxiety or depression like behavior. In summary, our study provides comprehensive data on how the impairment of neurogenesis caused by the loss of the cell fate determinant TRIM32 causes a decrease of olfactory performance as well as a deregulation of metabolomic pathways that are linked to mood disorders.
在哺乳动物中,新神经元在整个生命周期内于大脑的两个特定区域产生,即海马体的齿状回(DG)和脑室下区(SVZ)-嗅球(OB)系统。在这两个区域,新生神经元表现出独特的特性,使其与成熟神经元明显区分开来。增强的兴奋性和增加的突触可塑性使它们能够通过调节已建立的成熟神经元的现有局部回路,为信息处理增添特定特性。海马体神经发生被认为在空间导航学习、空间记忆和空间模式分离中发挥作用。越来越多的证据表明,成年后产生的OB神经元有助于学习过程和气味记忆。我们最近证明,细胞命运决定因子TRIM32在成年小鼠大脑SVZ-OB系统分化的神经母细胞中上调。TRIM32的缺失导致祖细胞增殖增加和细胞死亡减少。这两种效应共同导致成年后产生的OB神经元过度生成。在此,我们展示了行为学研究的新数据,表明这种OB神经发生的增强不一定会导致嗅觉能力提高,相反甚至会导致嗅觉能力受损。此外,我们在细胞水平上表明,TRIM32蛋白水平在神经干细胞(NSC)分化过程中增加。在分子水平上,与糖酵解、甘氨酸或半胱氨酸代谢相关的几种代谢中间体在TRIM32基因敲除小鼠的脑组织中失调。这些代谢组学途径直接或间接与焦虑或抑郁样行为相关。总之,我们的研究提供了全面的数据,说明细胞命运决定因子TRIM32的缺失导致神经发生受损如何引起嗅觉能力下降以及与情绪障碍相关的代谢组学途径失调。