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近日，来自华盛顿大学的科学家通过研究发现，一类在大脑中含量丰富的支持细胞在神经元之间的交流能力上扮演着重要角色，相关研究为开发抵御自闭症、精神分裂症及其它神经精神疾病的新型策略或提供了新的思路。
相关研究刊登于国际杂志Journal of Neuroscience上，研究者表示，在培养液中如果没有星形胶质细胞，神经元发送特殊信号的能力就会减弱，进而就会干扰神经元的发育，引发神经元之间交流出现问题，包括自闭症及精神分裂症的发生。文章第一作者Courtney Sobieski表示，本文研究表明，尽管神经元是很多研究都重点，但大脑中还包含有其它类型的细胞，对这些细胞进行研究也是非常重要的，星形胶质细胞是维持健康神经元发育的重要支持细胞，而如果没有星形胶质细胞，神经元之间的交流就会出现故障。
研究者表示，一种名为谷氨酸盐的神经递质在大脑中运输信息上扮演着重要角色，其在大脑90%的交流沟通中都是主要的神经递质，而且当移除星形胶质细胞后，谷氨酸盐信号就会减弱；Sobieski说道，我们在实验室中开发了一种方法，其可以在星形胶质细胞存在或不存在的情况下均生长出单一的神经元细胞，当没有星形胶质细胞时，神经元发送谷氨酸盐的能力就会减弱以及变得杂乱。
谷氨酸盐信号的减弱就会感染神经元的发育以及出现很多神经性问题，比如引发自闭症和精神分裂症的发生；和星形胶质细胞相关的谷氨酸盐信号的干扰和癫痫症发病直接相关，而癫痫症的主要特点为电信号被阻断。
最后研究者表示，后期还需要继续进行更多深入的研究，但超越神经元研究也显得更为重要，或许根本的问题和星形胶质细胞有关，因此扩大研究或许对于深入理解神经性疾病的发生机制会带来一定的思路和希望。
PMID:
Loss of Local Astrocyte Support Disrupts Action Potential Propagation and Glutamate Release Synchrony from Unmyelinated Hippocampal Axon Terminals In Vitro
Courtney Sobieski1,2, Xiaoping Jiang1, Devon C. Crawford1,2, and Steven Mennerick1,3,4
Neuron–astrocyte interactions are critical for proper CNS development and function. Astrocytes secrete factors that are pivotal for synaptic development and function, neuronal metabolism, and neuronal survival. Our understanding of this relationship, however, remains incomplete due to technical hurdles that have prevented the removal of astrocytes from neuronal circuits without changing other important conditions. Here we overcame this obstacle by growing solitary rat hippocampal neurons on microcultures that were comprised of either an astrocyte bed (+astrocyte) or a collagen bed (−astrocyte) within the same culture dish. −Astrocyte autaptic evoked EPSCs, but not IPSCs, displayed an altered temporal profile, which included increased synaptic delay, increased time to peak, and severe glutamate release asynchrony, distinct from previously described quantal asynchrony. Although we observed minimal alteration of the somatically recorded action potential waveform, action potential propagation was altered. We observed a longer latency between somatic initiation and arrival at distal locations, which likely explains asynchronous EPSC peaks, and we observed broadening of the axonal spike, which likely underlies changes to evoked EPSC onset. No apparent changes in axon structure were observed, suggesting altered axonal excitability. In conclusion, we propose that local astrocyte support has an unappreciated role in maintaining glutamate release synchrony by disturbing axonal signal propagation.