Rogerson-Wood Lara, Sawatari Atomu, Leamey Catherine A
School of Medical Sciences (Neuroscience theme), Faculty of Medicine and Health, University of Sydney, NSW 2006, Australia.
IBRO Neurosci Rep. 2025 Jun 5;19:91-100. doi: 10.1016/j.ibneur.2025.05.013. eCollection 2025 Dec.
Neural connectivity is essential for brain function: this is initially established via early axon guidance mechanisms and subsequently refined by synaptic pruning. Alterations in the patterns of neural connectivity, arising due to changes in either of these processes, are found in neurodevelopmental conditions. Microglia, the brain's resident immune cell, are recognised mediators of synaptic pruning. Unlike axon guidance, synaptic pruning occurs over protracted periods of postnatal life and can be profoundly impacted by experience. Little is known about whether targeted microglial synaptic pruning could be recruited to compensate for alterations in neural connectivity arising due to deleterious changes in other neurodevelopmental processes, such as axon guidance. Here we review our recent work which has addressed this by examining the effect of Environmental Enrichment (EE) on the miswired visual circuitry of mice lacking the axon guidance molecule Ten-m3. Notably, exposure to EE commenced around birth (but not from weaning or later) triggered selective removal of miswired retinal inputs in the visual thalamus of these Ten-m3 knockout mice. Most importantly, our work identifies selective microglial engulfment of neural connections during a defined postnatal window, as a likely mediator of this effect of early EE. The findings reviewed here emphasise the importance of early life experience in shaping neural circuitry, particularly when early development has been compromised by genetic factors. They also provide a potential mechanistic underpinning for the results of recent clinical trials investigating the effectiveness of early, experience-based interventions for human neurodevelopmental conditions.
其最初通过早期轴突导向机制建立,随后通过突触修剪得以完善。在神经发育疾病中可发现,由于这两个过程中任何一个发生变化而导致的神经连接模式改变。小胶质细胞作为大脑中的常驻免疫细胞,是公认的突触修剪调节因子。与轴突导向不同,突触修剪在出生后的很长一段时间内发生,并且会受到经验的深刻影响。关于是否可以利用靶向性小胶质细胞突触修剪来补偿因其他神经发育过程(如轴突导向)中的有害变化而引起的神经连接改变,目前知之甚少。在此,我们回顾了我们最近的研究工作,该工作通过研究环境富集(EE)对缺乏轴突导向分子Ten-m3的小鼠视觉回路错连的影响来解决这一问题。值得注意的是,在出生左右开始(而非从断奶期或更晚开始)接触EE会触发这些Ten-m3基因敲除小鼠视觉丘脑中错连视网膜输入的选择性清除。最重要的是,我们的研究确定了在特定的出生后窗口期内,神经连接的选择性小胶质细胞吞噬是早期EE产生这种效应的可能调节因子。本文回顾的研究结果强调了早期生活经历在塑造神经回路中的重要性,尤其是当早期发育受到遗传因素影响时。它们还为最近关于基于经验的早期干预对人类神经发育疾病有效性的临床试验结果提供了潜在的机制基础。