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电压门控钠离子通道scn1Laa参与斑马鱼脑神经发育和运动行为调节的研究
引用本文:何雪,王雨果,郑奕,黄亚娟,鲍宝龙.电压门控钠离子通道scn1Laa参与斑马鱼脑神经发育和运动行为调节的研究[J].上海海洋大学学报,2022,31(5):1057-1067.
作者姓名:何雪  王雨果  郑奕  黄亚娟  鲍宝龙
作者单位:上海海洋大学 水产种质资源发掘与利用教育部重点实验室;上海海洋大学 水产科学国家级实验教学示范中心,上海海洋大学 水产种质资源发掘与利用教育部重点实验室;上海海洋大学 水产科学国家级实验教学示范中心,上海海洋大学 水产科学国家级实验教学示范中心,上海海洋大学 水产种质资源发掘与利用教育部重点实验室;上海海洋大学 水产科学国家级实验教学示范中心,上海海洋大学 水产种质资源发掘与利用教育部重点实验室;上海海洋大学 水产科学国家级实验教学示范中心
基金项目:国家自然科学基金面上项目(31872546)
摘    要:电压门控钠离子通道对于脊椎动物脑神经起始、传播动作电位具有重要作用。为了解斑马鱼电压门控钠离子通道基因scn1Laa在脑神经中的作用,通过CRISPR/Cas9基因编辑技术,首次构建了可稳定遗传的生长没有受明显影响的scn1Laa缺陷型(scn1Laa-/-)斑马鱼家系。相比野生型,5 dpf(days post-fertilization,受精后5天)scn1Laa缺陷型斑马鱼兴奋抑制性神经元(氨基丁酸类神经元)表达相对增加,兴奋类神经元(谷氨酸能类神经元)和成熟神经元显著减少,脑部细胞增殖也显著减少。受精后5天和90 天的 scn1Laa缺陷型斑马鱼的运动较同时期野生型斑马鱼更为活跃,受精后90天的 scn1Laa缺陷型斑马鱼的运动具有明显的爆发性。以上结果表明,scn1laa缺失导致兴奋类神经元(谷氨酸能类神经元)以及神经细胞增殖减少,影响脑周围神经放电,导致运动神经调节障碍,出现运动行为异常活跃。即电压门控钠离子通道基因scn1Laa参与斑马鱼脑神经发育和生长,间接参与运动行为调节。同时本文也为进一步探究电压门控钠离子通道在脑神经中的作用奠定基础。

关 键 词:电压门控钠离子通道,scn1Laa,斑马鱼,基因编辑,脑神经,爆发性运动,生长
收稿时间:2021/7/28 0:00:00
修稿时间:2021/11/16 0:00:00

Voltage-gated sodium channel scn1Laa is involved in the development of zebrafish cranial nerves and the regulation of motor behavior
HE Xue,WANG Yuguo,ZHENG Yi,HUANG Yajuan,BAO Baolong.Voltage-gated sodium channel scn1Laa is involved in the development of zebrafish cranial nerves and the regulation of motor behavior[J].Journal of Shanghai Ocean University,2022,31(5):1057-1067.
Authors:HE Xue  WANG Yuguo  ZHENG Yi  HUANG Yajuan  BAO Baolong
Institution:Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources,Ministry of Education,Shanghai;National Demonstration Center for Experimental Fisheries Science Education,Shanghai Ocean University,Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources,Ministry of Education,Shanghai;National Demonstration Center for Experimental Fisheries Science Education,Shanghai Ocean University,National Demonstration Center for Experimental Fisheries Science Education,Shanghai Ocean University,Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources,Ministry of Education,Shanghai;National Demonstration Center for Experimental Fisheries Science Education,Shanghai Ocean University,Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources,Ministry of Education,Shanghai;National Demonstration Center for Experimental Fisheries Science Education,Shanghai Ocean University
Abstract:Voltage-gated sodium channels ((VGSC) play an important role in the initiation and propagation of action potentials in vertebrate cranial nerves. To investigate the role of zebrafish Voltage-gated sodium channel member scn1Laa in cranial nerves, the CRISPR/Cas9 approach was used to establish a stable hereditary scn1Laa-deficient (scn1Laa-/-) zebrafish without significant defect on growth. Compared with wild-type siblings, there are more GABAergic neurons (inhibitory neurons) in scn1Laa-deficient larvae at 5 dpf (5 days post-fertilization), while glutamatergic (excitatory neurons) and mature neurons are significantly reduced. Besides, cell proliferation in the brain is also reduced at 5 dpf. The movement of scn1Laa-deficient zebrafish at 5 or 90 dpf was more active than that of wild-type siblings at the same time, and the burst movement of scn1Laa-deficient zebrafish was observed at 90 dpf. These results showed that loss of scn1laa leads to excitatory neurons (glutamatergic neurons) increase and reduced cell proliferation of cranial nerve, which affect the discharge of peripheral nerve, cause motor nerve dysfunction and abnormal motor behavior. Above all, the voltage-gated sodium channel scn1Laa participates in the development and functional maintenance of the zebrafish cranial nerve and indirectly participates in the regulating behavior with limited influence on body growth. At the same time, this research also lays the foundation for further exploration of voltage-gated sodium channels in the cranial nerves.
Keywords:Voltage-gated sodium channels  scn1Laa  zebrafish  gene editing  cranial nerves  burst movement  growth
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