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蝗虫中枢神经系统中扩散性抑制的应激预处理

Stress preconditioning of spreading depression in the locust CNS.

作者信息

Rodgers Corinne I, Armstrong Gary A B, Shoemaker Kelly L, LaBrie John D, Moyes Christopher D, Robertson R Meldrum

机构信息

Department of Biology, Queen's University, Biosciences Complex, Kingston, Ontario, Canada.

出版信息

PLoS One. 2007 Dec 26;2(12):e1366. doi: 10.1371/journal.pone.0001366.

DOI:10.1371/journal.pone.0001366
PMID:18159249
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2137934/
Abstract

Cortical spreading depression (CSD) is closely associated with important pathologies including stroke, seizures and migraine. The mechanisms underlying SD in its various forms are still incompletely understood. Here we describe SD-like events in an invertebrate model, the ventilatory central pattern generator (CPG) of locusts. Using K(+) -sensitive microelectrodes, we measured extracellular K(+) concentration (K(+)) in the metathoracic neuropile of the CPG while monitoring CPG output electromyographically from muscle 161 in the second abdominal segment to investigate the role K(+) in failure of neural circuit operation induced by various stressors. Failure of ventilation in response to different stressors (hyperthermia, anoxia, ATP depletion, Na(+)/K(+) ATPase impairment, K(+) injection) was associated with a disturbance of CNS ion homeostasis that shares the characteristics of CSD and SD-like events in vertebrates. Hyperthermic failure was preconditioned by prior heat shock (3 h, 45 degrees C) and induced-thermotolerance was associated with an increase in the rate of clearance of extracellular K(+) that was not linked to changes in ATP levels or total Na(+)/K(+) ATPase activity. Our findings suggest that SD-like events in locusts are adaptive to terminate neural network operation and conserve energy during stress and that they can be preconditioned by experience. We propose that they share mechanisms with CSD in mammals suggesting a common evolutionary origin.

摘要

皮层扩散性抑制(CSD)与包括中风、癫痫和偏头痛在内的重要病理状况密切相关。其各种形式的扩散性抑制背后的机制仍未完全明了。在此,我们描述了一种无脊椎动物模型——蝗虫的呼吸中枢模式发生器(CPG)中的类扩散性抑制事件。我们使用对钾离子(K⁺)敏感的微电极,在监测来自第二腹节肌肉161的CPG输出肌电图的同时,测量CPG后胸神经纤维网中的细胞外钾离子浓度([K⁺]ₒ),以研究钾离子在各种应激源诱导的神经回路运作失灵中的作用。对不同应激源(高热、缺氧、ATP耗竭、钠钾ATP酶损伤、钾离子注射)的呼吸反应失灵与中枢神经系统离子稳态的紊乱相关,这种紊乱具有脊椎动物中CSD和类扩散性抑制事件的特征。高热导致的呼吸反应失灵可由先前的热休克(3小时,45摄氏度)预处理,诱导性热耐受与细胞外钾离子清除率的增加相关,而这与ATP水平或总钠钾ATP酶活性的变化无关。我们的研究结果表明,蝗虫中的类扩散性抑制事件是适应性的,可在应激期间终止神经网络运作并保存能量,并且它们可由经历进行预处理。我们提出,它们与哺乳动物中的CSD具有共同机制,这表明存在共同的进化起源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/19a1366ff2af/pone.0001366.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/20b018999094/pone.0001366.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/9c266d640eeb/pone.0001366.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/6c5593941155/pone.0001366.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/32ef9ee69c3b/pone.0001366.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/ef4e0e572b98/pone.0001366.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/d86a455c2c56/pone.0001366.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/19a1366ff2af/pone.0001366.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/20b018999094/pone.0001366.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/9c266d640eeb/pone.0001366.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/6c5593941155/pone.0001366.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/32ef9ee69c3b/pone.0001366.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/ef4e0e572b98/pone.0001366.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/d86a455c2c56/pone.0001366.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b9a/2137934/19a1366ff2af/pone.0001366.g007.jpg

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