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温度调节由抑制性谷氨酸信号介导的突触亚细胞特异性。

Temperature regulates synaptic subcellular specificity mediated by inhibitory glutamate signaling.

机构信息

Department of Neurosurgery, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Zhongshan Hospital, Fudan University, Shanghai, China.

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.

出版信息

PLoS Genet. 2021 Jan 11;17(1):e1009295. doi: 10.1371/journal.pgen.1009295. eCollection 2021 Jan.

DOI:10.1371/journal.pgen.1009295
PMID:33428618
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7822552/
Abstract

Environmental factors such as temperature affect neuronal activity and development. However, it remains unknown whether and how they affect synaptic subcellular specificity. Here, using the nematode Caenorhabditis elegans AIY interneurons as a model, we found that high cultivation temperature robustly induces defects in synaptic subcellular specificity through glutamatergic neurotransmission. Furthermore, we determined that the functional glutamate is mainly released by the ASH sensory neurons and sensed by two conserved inhibitory glutamate-gated chloride channels GLC-3 and GLC-4 in AIY. Our work not only presents a novel neurotransmission-dependent mechanism underlying the synaptic subcellular specificity, but also provides a potential mechanistic insight into high-temperature-induced neurological defects.

摘要

环境因素,如温度,会影响神经元的活动和发育。然而,目前尚不清楚它们是否以及如何影响突触亚细胞特异性。在这里,我们使用线虫秀丽隐杆线虫的 AIY 中间神经元作为模型,发现高温培养会通过谷氨酸能神经传递强烈诱导突触亚细胞特异性缺陷。此外,我们确定功能谷氨酸主要由 ASH 感觉神经元释放,并由 AIY 中的两个保守抑制性谷氨酸门控氯离子通道 GLC-3 和 GLC-4 感知。我们的工作不仅提出了一个新的突触亚细胞特异性的神经传递依赖机制,而且为高温诱导的神经缺陷提供了一个潜在的机制见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab42/7822552/9dfb292835bf/pgen.1009295.g008.jpg
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