Somjen G G, Aitken P G
An Acad Bras Cienc. 1984 Dec;56(4):495-504.
No complete picture of LD has emerged from these observations, but a general outline does seem to be sketched out. The missing details can, at present, be filled only with speculation. Leão's depression is a process that can be initiated by a wide variety of violent insults, mechanical, electrical or chemical. It often is preceded by paroxysmal discharge, but the occurrence of a seizure is not a necessary condition for its initiation. If it is started at one point it slowly spreads and its propagation is possible even through zones of gray matter in which impulse generation by neurons is blocked by TTX. LD is always associated with cell swelling and with a drastic redistribution of ions, which suggest a sieve-like increase of permeability of cell membranes. In most cases of LD, neurons are depolarized to the point where all electric signalling becomes impossible, but in some instances depolarization remains incomplete, or it is not evenly distributed over the neuron's surface, enabling continued generation of potential waves even though action potentials are blocked. Strong oxidation of NADH to NAD, and the accumulation of much acid in the interstitial fluid, indicate the intense metabolic activity during and after an episode of LD, presumably as cells work to restore the normal distribution of ions and the integrity of their membranes. What starts this process in the first place? Most observations are compatible with the hypothesis first proposed by Van Harreveld, suggesting that the release from cells of an endogenous substance might initiate LD. This auto-toxin may be, but need not be, an excitant amino acid. It is also possible that more than one substance may be involved; perhaps two or more agents must cooperate to create the conditions for LD, and such a need for the simultaneous action of more than one factor could explain the unpredictability of its eruption. The curious immunity of the spinal cord to LD may be due to the absence of one of the endo-toxins required for its initiation. Elsewhere in the brain and in the retina this hypothetical agent or agents may be present in both glial and neuronal elements. Any violent insult would cause its (or their) spillage into interstitial fluid. Once released from a few cells it (they) would impair the continence of the membranes of other cells and thus cause them to release their content of ions and with it their own dose of the auto-poison.(ABSTRACT TRUNCATED AT 400 WORDS)
从这些观察结果中，尚未形成关于去极化抑制（LD）的完整图景，但一个大致轮廓似乎已被勾勒出来。目前，缺失的细节只能靠推测来填补。利奥氏抑郁是一个可由多种暴力损伤引发的过程，包括机械、电或化学损伤。它通常先有阵发性放电，但癫痫发作并非其起始的必要条件。如果它在某一点开始，就会缓慢扩散，甚至可以通过神经元冲动产生被河豚毒素（TTX）阻断的灰质区域进行传播。去极化抑制总是与细胞肿胀以及离子的剧烈重新分布相关，这表明细胞膜的通透性呈筛状增加。在大多数去极化抑制的情况下，神经元去极化到所有电信号传导都无法进行的程度，但在某些情况下，去极化仍不完全，或者在神经元表面分布不均匀，即使动作电位被阻断，仍能持续产生电位波。烟酰胺腺嘌呤二核苷酸（NADH）强烈氧化为烟酰胺腺嘌呤二核苷酸（NAD），以及间质液中大量酸的积累，表明去极化抑制发作期间及之后存在强烈的代谢活动，大概是因为细胞努力恢复离子的正常分布及其膜的完整性。首先是什么启动了这个过程呢？大多数观察结果与范·哈勒维尔德最初提出的假设相符，即细胞释放一种内源性物质可能引发去极化抑制。这种自身毒素可能是，但不一定是，一种兴奋性氨基酸。也有可能不止一种物质参与其中；也许两种或更多的因子必须协同作用才能为去极化抑制创造条件，而这种对多种因子同时作用的需求可以解释其爆发的不可预测性。脊髓对去极化抑制的奇特免疫可能是由于缺乏其起始所需的一种内毒素。在大脑和视网膜的其他部位，这种假设的一种或多种因子可能同时存在于神经胶质细胞和神经元中。任何暴力损伤都会导致其（或它们）泄漏到间质液中。一旦从少数细胞中释放出来，它（们）就会损害其他细胞膜的通透性，从而导致它们释放离子含量以及自身剂量的自毒物质。（摘要截断于400字）
