AP2γ:成人海马神经发生调控的新参与者

Journal of Experimental Neuroscience Pub Date : 2018-04-02 eCollection Date: 2018-01-01 DOI:10.1177/1179069518766897
Antonio Mateus-Pinheiro, Nuno Dinis Alves, Nuno Sousa, Luisa Pinto
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引用次数: 4

摘要

自从认识到哺乳动物的大脑在整个生命过程中保持产生具有功能相关性的新生神经元的能力以来,控制成年神经发生的分子调节基质一直是人们关注的焦点。在最近发表在《分子精神病学》上的一项研究中,我们证明了激活蛋白2γ (AP2γ),一种先前涉及发育皮层中细胞命运决定的转录因子,在调节成人海马中谷氨酸能神经发生方面发挥了新的作用。使用不同的实验方法,我们发现AP2γ特异性存在于瞬时扩增祖细胞亚群中,在那里它作为成年出生的谷氨酸能颗粒神经元增殖和分化的关键促进子。引人注目的是,成人大脑中AP2γ的缺乏会损害新的谷氨酸能神经元的产生,从而影响皮质-边缘回路的功能。在这里,我们分享了我们对AP2γ如何整合成人海马中谷氨酸能神经发生的转录协调的看法,以及它如何作为一种新的候选分子,在稳态和神经病理环境中研究环境压力转化为脑神经可塑性的改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

AP2γ: A New Player on Adult Hippocampal Neurogenesis Regulation.

AP2γ: A New Player on Adult Hippocampal Neurogenesis Regulation.

AP2γ: A New Player on Adult Hippocampal Neurogenesis Regulation.

AP2γ: A New Player on Adult Hippocampal Neurogenesis Regulation.

Since the recognition that the mammalian brain retains the ability to generate newborn neurons with functional relevance throughout life, the matrix of molecular regulators that govern adult neurogenesis has been the focus of much interest. In a recent study published in Molecular Psychiatry, we demonstrate Activating Protein 2γ (AP2γ), a transcription factor previously implicated in cell fate determination in the developing cortex, as a novel player in the regulation of glutamatergic neurogenesis in the adult hippocampus. Using distinct experimental approaches, we showed that AP2γ is specifically present in a subpopulation of transient amplifying progenitors, where it acts as a crucial promoter of proliferation and differentiation of adult-born glutamatergic granule neurons. Strikingly, deficiency of AP2γ in the adult brain compromises the generation of new glutamatergic neurons, with impact on the function of cortico-limbic circuits. Here, we share our view on how AP2γ integrates the transcriptional orchestration of glutamatergic neurogenesis in the adult hippocampus, and consequently, how it emerges as a novel molecular candidate to study the translation of environmental pressures into alterations of brain neuroplasticity in homeostatic, but also in neuropathological contexts.

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