Thermal stress and neural function: adaptive mechanisms in insect model systems
Thermal stress and neural function: adaptive mechanisms in insect model systems
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DOI：
10.1016/j.jtherbio.2004.08.073
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发表时间：
2004-10-01
影响因子：
2.7
通讯作者：
Robertson, RM
中科院分区：
文献类型：
--
作者：
Robertson, RM
神经回路的功能很容易受到高温的破坏，但可以通过应激预处理来保护，例如暴露于短暂的亚致死高温热激蛋白（HSP）的表达增加，热激蛋白（HSP）的表达增加，热激蛋白（HSP）的表达增加，特别是HSP 70。通过增加HSP 70基因的剂量来增强HSP 70的表达并不能改善果蝇HS诱导的幼虫运动或运动中枢模式产生的热耐受性。先前的应激下调神经元K+电流，这与动作电位时程的适应性增加有关。蝗虫中枢模式产生器的高温失效和恢复与细胞外K+的灾难性增加密切相关。这些和其他数据表明，神经回路功能可以通过应激诱导的HSP上调来保护，HSP稳定细胞骨架并保持重要的膜蛋白如离子通道、受体和Na+/K+-ATP酶的操作。(C)2004爱思唯尔有限公司保留所有权利。
Neural circuit function is vulnerable to hyperthermic failure but can be protected by stress pretreatments, such as exposure to a brief, sub-lethal high temperature (heat shock, HS), by increasing the time to failure and decreasing the time to recover.Insects provide excellent model systems to investigate potential mechanisms underlying thermotolerant operation.Induced thermotolerance is mediated by increased expression of heat shock proteins, HSPs, notably HSP70. Enhanced expression of HSP70 by increasing the gene dosage does not improve HS-induced thermotolerance of larval locomotion or locomotor central pattern generation in Drosophila.Prior stress down-regulates neuronal K+ currents and this is associated with adaptive increases in the duration of action potentials.Hyperthermic failure and recovery of the ventilatory central pattern generator in locusts is tightly correlated with a catastrophic increase in extracellular K+ concentration and its subsequent restoration.These, and other data, suggest that neural circuit function can be protected by a stress-induced upregulation of HSPs that stabilize the cytoskeleton and preserve the operation of important membrane proteins such as ion channels, receptors and the Na+/K+-ATPase. (C) 2004 Elsevier Ltd. All rights reserved.