Amemori T, Bures J
Neurosci Lett. 1986 Nov 21;71(3):323-8. doi: 10.1016/0304-3940(86)90641-5.
The time course of terminal anoxic depolarization and of the concomitant [K+]e increase was compared in the cerebral cortex and olfactory bulb of rats anesthetized with pentobarbital. Respiration arrest elicited by (+)-tubocurarine induced a negative slow potential shift which reached 50% of maximum after 90 s in the cortex and after 180 s in the olfactory bulb (n = 10). Bulbar [K+]e increased slowly to 16 mmol/l, then more rapidly to 40 60 mmol/l and reached 90 mmol/l after 10 min asphyxia (n = 10). While the resting and maximal [K+]e levels were the same in the cortex and olfactory bulb, the fast [K+]e rise started in the olfactory bulb at a higher level (16 mmol/l) and proceeded at a slower rate (doubling time 14 s) than in the cortex, where the same values were 11 mmol/l and 5 s, respectively. It is argued that the olfactory bulb resistance to asphyxia is due to a powerful GABAergic inhibition which counteracts the autoregenerative ionic shift and accounts for the absence of spreading depression in this structure.
在戊巴比妥麻醉的大鼠大脑皮层和嗅球中，比较了终末期缺氧去极化和伴随的细胞外钾离子浓度升高的时间进程。由筒箭毒碱引发的呼吸停止导致负性慢电位变化，在皮层中90秒后达到最大值的50%，在嗅球中180秒后达到最大值的50%（n = 10）。嗅球细胞外钾离子浓度缓慢升高至16 mmol/L，然后更快地升至40 - 60 mmol/L，并在窒息10分钟后达到90 mmol/L（n = 10）。虽然皮层和嗅球中的静息和最大细胞外钾离子浓度水平相同，但嗅球中细胞外钾离子的快速升高起始水平较高（16 mmol/L），且速率比皮层慢（加倍时间14秒），皮层中的起始水平和加倍时间分别为11 mmol/L和5秒。有人认为，嗅球对窒息的耐受性归因于强大的γ-氨基丁酸能抑制作用，这种抑制作用抵消了自动再生性离子转移，并解释了该结构中不存在扩散性抑制的原因。
