Suppression of evoked potentials with continued ion transport during anoxia in turtle brain.

Suppression of evoked potentials with continued ion transport during anoxia in turtle brain.
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龟脑缺氧期间持续离子传输对诱发电位的抑制。

DOI:
10.1152/ajpregu.1988.255.3.r478
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发表时间:
1988
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Sick,TJ
Sick,TJ
中科院分区:
--
文献类型:
--
作者:
Feng,ZC;Rosenthal,M;Sick,TJ

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龟脑在缺氧时存活的关键是持续的离子转运和避免缺氧去极化。以前的研究结果表明,ATP浓度保持不变,在长期缺氧和计算,ATP生产减少表明,代偿过程,而不是消耗能量储存或增加无氧糖酵解,也必须有助于离子稳态和脑存活。为了确定离子转运的保存是否与氧化代谢丧失期间的电生理学变化相关,电刺激戊巴比妥钠麻醉的海龟的大脑,1)引起细胞外K+活性的可测量的增加(a度k)用于确定刺激部位K+再蓄积的速率; 2)用于引起多突触胞外场电位(诱发电位)记录在嗅球。在缺氧,基线a度k上升只有几个毫摩尔,和速率的再积累的K+,增加刺激略有放缓,但不显着。与此相反,嗅球颗粒细胞的突触后顺向反应显着抑制缺氧。颗粒细胞对外侧嗅束逆向刺激的单突触反应受影响较小,嗅神经复合动作电位不受缺氧影响。这些数据表明,与哺乳动物一样,龟脑中的突触传递高度依赖于氧化代谢,并且龟脑可以通过抑制电活动来有效地保存缺氧期间离子转运的能量。
A key to turtle brain survival during anoxia is continued ion transport and avoidance of anoxic depolarization. Previous findings that ATP concentration remained constant during prolonged anoxia and calculations that ATP production decreased indicate that compensatory processes, other than consumption of energy stores or increased anaerobic glycolysis, must also contribute to ion homeostasis and brain survival. To determine whether preservation of ion transport is associated with changes in electrophysiology during loss of oxidative metabolism, the brains of pentobarbital sodium-anesthetized turtles were electrically stimulated 1) to provoke measurable increments in extracellular K+ activity (a degrees k) for determination of rates of K+ reaccumulation at the stimulus site and 2) to elicit polysynaptic extracellular field potentials (evoked potentials) recordable in the olfactory bulb. During anoxia, base-line a degrees k rose only a few millimolar, and rates of reaccumulation of K+, incremented by stimulation were slightly but not significantly slowed. In contrast, postsynaptic orthodromic responses of olfactory bulb granule cells were markedly depressed by anoxia. Monosynaptic responses of granule cells to antidromic stimulation of the lateral olfactory tract were less affected, and compound action potentials in the olfactory nerve were unchanged by anoxia. These data suggest that synaptic transmission in turtle brain, as in that of mammal, is highly dependent on oxidative metabolism and that the turtle brain may effectively conserve energy for ion transport during anoxia by depression of electrical activity.
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