中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (10): 1992-1993.doi: 10.4103/1673-5374.308082

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

范式转变:小胶质细胞(非神经元细胞)在学习和记忆中的新兴作用

  

  • 出版日期:2021-10-15 发布日期:2021-03-19

A paradigm shift: emerging roles of microglia, a non-neuronal cell, in learning and memory

Neelima Gupta, S. Thameem Dheen*   

  1. Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore,  Singapore 
  • Online:2021-10-15 Published:2021-03-19
  • Contact: S. Thameem Dheen, PhD, antstd@nus.edu.sg.
  • Supported by:
    In order to comply with the limited space, we apologize for not citing most of the work presented here done by our colleagues in the field. 

    This work was supported by the NUS Strategic Research Grant (Memory Networks in Rodent and Primate) DPRT/944/09/14 (R185-000-271-646) (to STD) and Ministry of Education (Tier 2) grant (R181-000-186-112) (to STD). 

摘要:

Neural Regen Res:靶向小胶质细胞信号通路可能是治疗神经退行性疾病的潜在方法之一

 

小胶质细胞是非神经元细胞,可抵御各种中枢神经系统(CNS)损伤。它们充当哨兵,通过其在CNS中的分支在周围薄壁组织中不间断地巡逻。病理学损伤后,小胶质细胞被激活、增殖、迁移到损伤或感染部位,释放趋化因子和细胞因子,随后吞噬死细胞和碎片。

 

来自新加坡国立大学的S. Thameem Dheen团队最近的研究表明小胶质磷脂酰肌醇3激酶(PI3K/蛋白激酶BAKT/脑源性神经营养因子(BDNF)途径在长期增强(LTP)中起着关键作用,形成了学习和记忆的细胞基础。尽管神经元PI3K / AKT途径通过BDNF参与突触可塑性,但小胶质PI3K / AKT途径已被初步证明对小胶质细胞的炎症反应至关重要。小胶质细胞PI3K / AKT-BDNF通路对于LTP是必不可少的,可以调节健康大脑中的LTP。团队在另一项研究关注活化的原代大鼠小神经胶质细胞进行的miRNA微阵列中,假定靶向钙/钙调蛋白依赖性蛋白激酶2aCamk2a)基因的3'UTRmiRNA-142家族在活化的小胶质细胞(Gupta)中的表达显着上调。Dr. Dheen及其团队认为操纵或改变小胶质细胞功能的治疗策略可能是减轻认知能力下降的有效方法,靶向小胶质细胞信号通路可能是神经退行性疾病治疗中一种有效的替代或补充方法,具有调节突触传递和可塑性的潜力。但还需对神经退行性疾病动物模型进行进一步的体内研究,以确定小胶质细胞对神经退行性疾病中LTP和突触可塑性的贡献程度。

 

 

 

文章在《中国神经再生研究(英文版)》杂志20211010期发表。

https://orcid.org/0000-0001-9600-6789 (S. Thameem Dheen)

Abstract: Microglial cells are non-neuronal cells which serve as the first line of defence against various injuries and insults in the central nervous system (CNS). They act as sentinels that constantly patrol the surrounding parenchyma through their ramified processes in the CNS. In response to any pathological insult, microglia become activated, undergo proliferation, migrate to the site of injury or infection, and release chemokines and cytokines followed by the phagocytosis of dead cells and debris.