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在ALS的多种模型中,在症状前阶段,刺激与抑制的突触比率没有变化

Calum Bonthron¹, Sarah Burley^1,2, Matthew J Broadhead¹

¹School of Psychology and Neuroscience, University of St Andrews, St Andrews, United Kingdom.

|August 1, 2024

概括

这项研究研究了氨基转移性侧面硬化症 (ALS) 中激发与抑制 (E:I) 突触比率. 研究人员在小鼠模型或人类细胞培养物中没有发现改变E:I比率的证据,这表明突触失衡不是早期ALS过度兴奋的主要驱动因素.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
神经退行性疾病神经退行性疾病

背景情况:

运动神经元过度兴奋是肌缩侧面硬化症 (ALS) 的早期标志.
改变激发与抑制 (E:I) 突触比率被假设为这种过度兴奋性作出贡献.
参与突触发生的星体细胞与ALS病变产生有关,并可能影响突触平衡.

研究的目的:

为了调查E:I突触比是否在ALS早期阶段发生变化.
确定星体细胞在ALS潜在的突触失衡中的作用.
在老鼠模型和人类ALS细胞培养物中评估突触E:I比率.

主要方法:

利用来自新生小鼠和人类iPSC衍生的细胞的初级脊髓神经元/星细胞共同培养.
评估了E:I突触比率,使用突触前和突触后的解剖学标记.
分析了ALS小鼠脊髓灰质中的星细胞和E:I比率中的ephrin-B1表达.

主要成果:

在共同培养中没有观察到E:I突触比率的变化,不论是星球细胞或神经元基因型.
埃弗林-B1的表达并不是由ALS天体细胞差异调节的.
对ALS小鼠脊髓和人类ALS细胞培养物的分析显示,对刺激性或抑制性突触形成没有偏见.

结论:

该研究发现,在多个ALS模型中,激发性与抑制性突触的相对丰度没有显著变化.
这些发现表明,突触E:I比率的不平衡可能不是导致ALS早期运动神经元过度兴奋的主要原因.
天体细胞在ALS病原体中的突触失衡中的作用需要进一步研究.

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