Bures J, Buresová O
J Neurobiol. 1981 May;12(3):211-20. doi: 10.1002/neu.480120303.
The time course of the [K+]e increase elicited by terminal anoxia or by electroconvulsive shock (ECS) was compared in various parts of the rat brain. The [K+]e was measured with ion-selective microelectrodes stereotaxically introduced into the target area. Respiration arrest induced in anesthetized rats a slow [K+]e increase to about 6--10 mM followed by an abrupt rise to 30--50 mM (doubling time 5--14 sec) in the neocortex, hippocampus, amygdala, caudate nucleus, and thalamus. In the reticular formation, zona incerta, and lateral hypothalamus the second phase of [K+]e increase was much slower (doubling time 30--50 sec) and lacked the autoregenerative character. Trans-pinnate ECS (50 Hz, 0.5 sec, 80 mA), administered to rats immobilized with gallamine triethiodide, elicited a generalized [K+]e increase of the spreading depression type in neocortex and hippocampus (40 mM) as well as in the caudate nucleus and thalamus (20--30 mM), followed by slow [K+]e decrease (half-time 40--60 sec). Much lower ECS-induced [K+]e increase (to 5--6 mM) was observed in the reticular formation, zona incerta, lateral hypothalamus and, surprisingly, in the amygdala. It is concluded that the autoregenerative [K+]e release of spreading depression type develops in structures with high density of membranes reacting to partial depolarization by increased sodium permeability.
在大鼠大脑的不同部位比较了终末期缺氧或电惊厥休克（ECS）引起的细胞外钾离子浓度（[K⁺]e）升高的时间进程。使用立体定位插入靶区域的离子选择性微电极测量[K⁺]e。在麻醉大鼠中诱导呼吸停止会使新皮层、海马体、杏仁核、尾状核和丘脑中的[K⁺]e缓慢升高至约6 - 10 mM，随后突然升至30 - 50 mM（加倍时间5 - 14秒）。在网状结构、未定带和外侧下丘脑，[K⁺]e升高的第二阶段要慢得多（加倍时间30 - 50秒），并且缺乏自我再生特性。对用三碘季铵酚固定的大鼠施加经皮针状ECS（50 Hz，0.5秒，80 mA），会在新皮层和海马体（40 mM）以及尾状核和丘脑（20 - 30 mM）中引起扩散性抑制类型的全身性[K⁺]e升高，随后[K⁺]e缓慢下降（半衰期40 - 60秒）。在网状结构、未定带、外侧下丘脑以及令人惊讶的是在杏仁核中，观察到ECS诱导的[K⁺]e升高要低得多（至5 - 6 mM）。得出的结论是，扩散性抑制类型的自我再生性[K⁺]e释放在对部分去极化通过增加钠通透性做出反应的高密度膜结构中发展。
