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Fetal alcohol spectrum disorders model alters the functionality of glutamatergic neurotransmission in adult zebrafish.
NeuroToxicology ( IF 3.4 ) Pub Date : 2020-03-12 , DOI: 10.1016/j.neuro.2020.03.003 Suelen Baggio 1 , Kamila Zenki 1 , Alberto Martins Silva 1 , Thainá Garbino Dos Santos 1 , Giovana Rech 1 , Gabriela Lazzarotto 1 , Renato Dutra Dias 1 , Ben Hur Mussulini 2 , Eduardo Pacheco Rico 3 , Diogo Losch de Oliveira 1
NeuroToxicology ( IF 3.4 ) Pub Date : 2020-03-12 , DOI: 10.1016/j.neuro.2020.03.003 Suelen Baggio 1 , Kamila Zenki 1 , Alberto Martins Silva 1 , Thainá Garbino Dos Santos 1 , Giovana Rech 1 , Gabriela Lazzarotto 1 , Renato Dutra Dias 1 , Ben Hur Mussulini 2 , Eduardo Pacheco Rico 3 , Diogo Losch de Oliveira 1
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Fetal alcohol spectrum disorders (FASD) describe a wide range of ethanol-induced developmental disabilities, including craniofacial dysmorphology, and neurochemical and behavioral impairments. Zebrafish has become a popular animal model to evaluate the long-lasting effects of, both, severe and milder forms of FASD, including alterations to neurotransmission. Glutamate is one of the most affected neurotransmitter systems in ethanol-induced developmental disabilities. Therefore, the aim of the present study was to evaluate the functionality of the glutamatergic neurotransmitter system in an adult zebrafish FASD model. Zebrafish larvae (24 h post-fertilization) were exposed to ethanol (0.1 %, 0.25 %, 0.5 %, and 1%) for 2 h. After 4 months, the animals were euthanized and their brains were removed. The following variables were measured: glutamate uptake, glutamate binding, glutamine synthetase activity, Na+/K + ATPase activity, and high-resolution respirometry. Embryonic ethanol exposure reduced Na+-dependent glutamate uptake in the zebrafish brain. This reduction was positively modulated by ceftriaxone treatment, a beta-lactam antibiotic that promotes the expression of the glutamate transporter EAAT2. Moreover, the 0.5 % and 1% ethanol groups demonstrated reduced glutamate binding to brain membranes and decreased Na+/K + ATPase activity in adulthood. In addition, ethanol reduced glutamine synthetase activity in the 1% EtOH group. Embryonic ethanol exposure did not alter the immunocontent of the glutamate vesicular transporter VGLUT2 and the mitochondrial energetic metabolism of the brain in adulthood. Our results suggest that embryonic ethanol exposure may cause significant alterations in glutamatergic neurotransmission in the adult zebrafish brain.
中文翻译：
胎儿酒精光谱失调模型会改变成年斑马鱼的谷氨酸能神经传递功能。
胎儿酒精频谱异常（FASD）描述了多种由乙醇引起的发育障碍，包括颅面畸形，神经化学和行为障碍。斑马鱼已经成为一种流行的动物模型，用于评估严重和较轻形式的FASD的长期作用，包括神经传递的改变。谷氨酸是乙醇引起的发育障碍中受影响最大的神经递质系统之一。因此，本研究的目的是评估成年斑马鱼FASD模型中谷氨酸能神经递质系统的功能。将斑马鱼的幼虫（受精后24小时）暴露于乙醇（0.1％，0.25％，0.5％和1％）中2小时。4个月后，对动物实施安乐死并切除大脑。测量了以下变量：谷氨酸吸收，谷氨酸结合，谷氨酰胺合成酶活性，Na + / K + ATPase活性和高分辨率呼吸测定法。胚胎乙醇暴露减少了斑马鱼脑中Na +依赖性谷氨酸的摄取。头孢曲松治疗（一种促进谷氨酸转运蛋白EAAT2表达的β-内酰胺抗生素）对这种减少有积极的调节作用。此外，在成年期，0.5％和1％的乙醇基团减少了谷氨酸与脑膜的结合，并降低了Na + / K + ATPase的活性。此外，乙醇会降低1％EtOH组中的谷氨酰胺合成酶活性。胚胎乙醇暴露不会改变谷氨酸水泡转运蛋白VGLUT2的免疫含量和成年后大脑的线粒体能量代谢。
更新日期：2020-03-12
中文翻译：
胎儿酒精光谱失调模型会改变成年斑马鱼的谷氨酸能神经传递功能。
胎儿酒精频谱异常（FASD）描述了多种由乙醇引起的发育障碍，包括颅面畸形，神经化学和行为障碍。斑马鱼已经成为一种流行的动物模型，用于评估严重和较轻形式的FASD的长期作用，包括神经传递的改变。谷氨酸是乙醇引起的发育障碍中受影响最大的神经递质系统之一。因此，本研究的目的是评估成年斑马鱼FASD模型中谷氨酸能神经递质系统的功能。将斑马鱼的幼虫（受精后24小时）暴露于乙醇（0.1％，0.25％，0.5％和1％）中2小时。4个月后，对动物实施安乐死并切除大脑。测量了以下变量：谷氨酸吸收，谷氨酸结合，谷氨酰胺合成酶活性，Na + / K + ATPase活性和高分辨率呼吸测定法。胚胎乙醇暴露减少了斑马鱼脑中Na +依赖性谷氨酸的摄取。头孢曲松治疗（一种促进谷氨酸转运蛋白EAAT2表达的β-内酰胺抗生素）对这种减少有积极的调节作用。此外，在成年期，0.5％和1％的乙醇基团减少了谷氨酸与脑膜的结合，并降低了Na + / K + ATPase的活性。此外，乙醇会降低1％EtOH组中的谷氨酰胺合成酶活性。胚胎乙醇暴露不会改变谷氨酸水泡转运蛋白VGLUT2的免疫含量和成年后大脑的线粒体能量代谢。
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