Hou Nicholas, Armstrong Gary A B, Chakraborty-Chatterjee Munmun, Sokolowski Marla B, Robertson R Meldrum
Department of Biology, Queen's University, Kingston, Ontario, Canada; and.
Department of Ecology and Evolutionary Biology, University of Toronto, Toronto, Ontario, Canada.
J Neurophysiol. 2014 Aug 15;112(4):814-23. doi: 10.1152/jn.00201.2014. Epub 2014 May 21.
The sensitivity of insect nervous systems to anoxia can be modulated genetically and pharmacologically, but the cellular mechanisms responsible are poorly understood. We examined the effect of a heat shock pretreatment (HS) on the sensitivity of the locust (Locusta migratoria) nervous system to anoxia induced by water immersion. Prior HS made locusts more resistant to anoxia by increasing the time taken to enter a coma and by reducing the time taken to recover the ability to stand. Anoxic comas were accompanied by surges of extracellular potassium ions in the neuropile of the metathoracic ganglion, and HS reduced the time taken for clearance of excess extracellular potassium ions. This could not be attributed to a decrease in the activity of protein kinase G, which was increased by HS. In homogenates of the metathoracic ganglion, HS had only a mild effect on the activity of Na(+)-K(+)-ATPase. However, we demonstrated that HS caused a threefold increase in the immunofluorescent localization of the α-subunit of Na(+)-K(+)-ATPase in metathoracic neuronal plasma membranes relative to background labeling of the nucleus. We conclude that HS induced trafficking of Na(+)-K(+)-ATPase into neuronal plasma membranes and suggest that this was at least partially responsible for the increased resistance to anoxia and the increased rate of recovery of neural function after a disturbance of K(+) homeostasis.
昆虫神经系统对缺氧的敏感性可通过基因和药理学手段进行调节，但其背后的细胞机制却知之甚少。我们研究了热休克预处理（HS）对蝗虫（飞蝗）神经系统对水浸诱导缺氧敏感性的影响。预先进行热休克预处理可使蝗虫对缺氧更具抵抗力，方法是延长进入昏迷状态所需的时间，并缩短恢复站立能力所需的时间。缺氧昏迷伴随着后胸神经节神经纤维网中细胞外钾离子的激增，而热休克预处理缩短了清除过量细胞外钾离子所需的时间。这不能归因于蛋白激酶G活性的降低，热休克预处理反而使其活性增加。在后胸神经节匀浆中，热休克预处理对钠钾ATP酶的活性只有轻微影响。然而，我们证明，相对于细胞核的背景标记，热休克预处理使后胸神经元质膜中钠钾ATP酶α亚基的免疫荧光定位增加了三倍。我们得出结论，热休克预处理诱导钠钾ATP酶转运至神经元质膜，并认为这至少部分解释了对缺氧抵抗力的增加以及钾离子稳态紊乱后神经功能恢复速率的提高。
