Hypoxia can induce neural excitotoxicity in mammals, but this adverse effect has not been investigated in aquatic animals to date, especially in crustaceans. This study explored the induction effect and toxic mechanism of acute hypoxia stress (1.0 ± 0.1 mg dissolved oxygen /L) for 24 h on neural excitotoxicity in juvenile Chinese mitten crab, Eriocheir sinensis. The results showed that hemolymph glucose and serum lactic acid content were significantly increased, and the mRNA expression of crustacean hyperglycemic hormone and hypoxia-inducible factor 1α were significantly up-regulated in the hypoxia group compared with control. RNA-Seq results confirmed that acute hypoxia stress had a more significant impact on carbohydrate metabolism than lipid and protein metabolism. In addition, the TUNEL assay showed that the apoptosis rate of nerve cells was significantly higher in the hypoxia group than in the control, and similar trends were observed in the expression of apoptosis-related genes. RNA-Seq results also showed that acute hypoxia stress-induced neuronal apoptosis by regulating multiple apoptosis-related pathways. Moreover, free glutamate and GABA contents in the nerve tissue of thoracic ganglia were significantly higher in the hypoxia group than in the control group. Furthermore, the mRNA expression of NMDA related receptors was significantly up-regulated in the hypoxia group compared with the control. Similar trends were observed in the expression of calcium-dependent degrading enzymes and endogenous antioxidant-related proteins or enzymes. Meanwhile, the mRNA expression level of high-affinity neuronal glutamate transporter in the hypoxia group was significantly up-regulated compared with the control, whereas the vesicular glutamate transporter was significantly down-regulated. Furthermore, NMDA-R antagonists (MK-801 and Ro25–6981) injection showed that NMDA-R served as the bridge and core position of glutamate-induced neural neurotoxicity. This study provides a new perspective and theoretical guidance for exploring the regulation of hypoxic tolerance in E. sinensis.

缺氧可在哺乳动物中诱发神经兴奋性毒性，但迄今为止尚未在水生动物中研究这种不利影响，特别是在甲壳类动物中。本研究探讨急性缺氧应激（1.0 ± 0.1 mg 溶解氧/L）24 h对中华绒螯蟹幼年中华绒螯蟹神经兴奋性毒性的诱导作用和毒性机制。. 结果显示，与对照组相比，缺氧组血淋巴葡萄糖和血清乳酸含量显着升高，甲壳类高血糖激素和缺氧诱导因子1α的mRNA表达显着上调。RNA-Seq 结果证实，急性缺氧应激对碳水化合物代谢的影响比脂质和蛋白质代谢更显着。此外，TUNEL检测显示缺氧组神经细胞凋亡率明显高于对照组，凋亡相关基因表达也有相似趋势。RNA-Seq 结果还表明，急性缺氧应激通过调节多种凋亡相关通路诱导神经元凋亡。而且，低氧组胸神经节神经组织中游离谷氨酸和GABA含量显着高于对照组。此外，与对照组相比，缺氧组NMDA相关受体的mRNA表达显着上调。在钙依赖性降解酶和内源性抗氧化剂相关蛋白或酶的表达中观察到类似的趋势。同时，与对照组相比，缺氧组高亲和力神经元谷氨酸转运蛋白的mRNA表达水平显着上调，而囊泡型谷氨酸转运蛋白的mRNA表达水平显着下调。此外，NMDA-R 拮抗剂（MK-801 和 Ro25-6981）注射表明 NMDA-R 是谷氨酸诱导的神经神经毒性的桥梁和核心位置。E.中华。