Pék-Scott M, Lutz P L
Department of Biological Sciences, Florida Atlantic University, Boca Raton, Florida 33431, USA.
Am J Physiol. 1998 Dec;275(6):R2023-7. doi: 10.1152/ajpregu.1998.275.6.R2023.
There is wide speculation that ATP-sensitive K+ (KATP) channels serve a protective function in the mammalian brain, being activated during periods of energy failure. The aim of the present study was to determine if KATP channels also have a protective role in the anoxia-tolerant turtle brain. After ouabain administration, rates of change in extracellular K+ were measured in the telencephalon of normoxic and anoxic turtles (Trachemys scripta). The rate of K+ efflux was reduced by 50% within 1 h of anoxia and by 70% at 2 h of anoxia, and no further decrease was seen at 4 h of anoxia. The addition of the KATP channel blocker glibenclamide or 2,3-butanedione monoxime prevented the anoxia-induced decrease in K+ efflux during the first hour of anoxia, but the effect of these blockers was diminished at 2 h of anoxia and was not seen after 4 h of anoxia. This pattern of change in KATP channel blocker sensitivity can be related to a previously established temporary fall and subsequent recovery of tissue ATP during early anoxia. We suggest that activated KATP channels are involved in the downregulation of membrane ion permeability (channel arrest) during the initial energy crisis period but are switched off when the full anoxic state is established and tissue ATP levels have been restored. We also found that, in contrast to those in mammals, KATP channels are not a major route for K+ efflux in the energy-depleted turtle brain.
人们广泛推测，ATP敏感性钾离子（KATP）通道在哺乳动物大脑中发挥保护作用，在能量衰竭期间被激活。本研究的目的是确定KATP通道在耐缺氧海龟大脑中是否也具有保护作用。在给予哇巴因后，测量了常氧和缺氧海龟（滑龟）端脑中细胞外钾离子的变化率。缺氧1小时内钾离子外流率降低了50%，缺氧2小时时降低了70%，缺氧4小时时未见进一步下降。添加KATP通道阻滞剂格列本脲或2,3-丁二酮单肟可在缺氧的第一小时内阻止缺氧诱导的钾离子外流减少，但这些阻滞剂的作用在缺氧2小时时减弱，缺氧4小时后未见作用。KATP通道阻滞剂敏感性的这种变化模式可能与先前确定的早期缺氧期间组织ATP的暂时下降和随后的恢复有关。我们认为，激活的KATP通道在初始能量危机期间参与膜离子通透性的下调（通道阻滞），但在完全缺氧状态建立且组织ATP水平恢复后会关闭。我们还发现，与哺乳动物不同，KATP通道不是能量耗尽的海龟大脑中钾离子外流的主要途径。
