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Preconditioning of Caenorhabditis elegans to anoxic insult by inactivation of cholinergic, GABAergic and muscle activity
Genes, Brain and Behavior ( IF 2.4 ) Pub Date : 2020-11-05 , DOI: 10.1111/gbb.12713
Heather L Bennett 1, 2, 3 , Patrick D McClanahan 4, 5 , Christopher Fang-Yen 4, 5 , Robert G Kalb 1, 2, 6
Affiliation  

For most metazoans, oxygen deprivation leads to cell dysfunction and if severe, death. Sublethal stress prior to a hypoxic or anoxic insult (“preconditioning”) can protect cells from subsequent oxygen deprivation. The molecular mechanisms by which sublethal stress can buffer against a subsequent toxic insult and the role of the nervous system in the response are not well understood. We studied the role of neuronal activity preconditioning to oxygen deprivation in Caenorhabditis elegans. Animals expressing the histamine gated chloride channels (HisCl1) in select cell populations were used to temporally and spatially inactivate the nervous system or tissue prior to an anoxic insult. We find that inactivation of the nervous system for 3 h prior to the insult confers resistance to a 48‐h anoxic insult in 4th‐stage larval animals. Experiments show that this resistance can be attributed to loss of activity in cholinergic and GABAergic neurons as well as in body wall muscles. These observations indicate that the nervous system activity can mediate the organism's response to anoxia.

中文翻译:


通过灭活胆碱能、GABA能和肌肉活动来预处理秀丽隐杆线虫以应对缺氧损伤



对于大多数后生动物来说,缺氧会导致细胞功能障碍,严重时甚至会导致死亡。缺氧或缺氧损伤之前的亚致死应激(“预处理”)可以保护细胞免受随后的缺氧影响。亚致死应激可以缓冲随后的毒性损伤的分子机制以及神经系统在反应中的作用尚不清楚。我们研究了秀丽隐杆线虫神经元活动预处理对缺氧的作用。在选择的细胞群中表达组胺门控氯离子通道(HisCl1)的动物被用来在缺氧损伤之前在时间和空间上使神经系统或组织失活。我们发现,在损伤前使神经系统失活 3 小时,可赋予第四阶段幼虫动物对 48 小时缺氧损伤的抵抗力。实验表明,这种抵抗可归因于胆碱能和 GABA 能神经元以及体壁肌肉的活性丧失。这些观察结果表明,神经系统活动可以介导生物体对缺氧的反应。
更新日期:2020-11-05
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