垂体激素和健忘症。

H Rigter, H Van Riezen
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引用次数: 0

摘要

脑下垂体激素通过对大脑的直接作用深刻地影响行为。这些行为效应之一是实验性健忘症的衰减。传统上,健忘症被认为是“记忆的丧失”。记忆至少包括两个阶段:输入(记忆巩固)和输出(记忆检索)。从理论上讲,任何方面的记忆障碍都可能是导致健忘症的原因。此外,健忘症也有可能是由一个或多个与记忆无关的因素造成的。回顾了有关人类健忘症的资料和理论。文中提到了一些显著特征:(1)健忘症可由多种药物引起;(2)健忘症持续时间从几秒钟到几年不等;(3)可以建立健忘症梯度;(4)健忘症在很大程度上是可逆的。从这一调查来看,失忆症似乎不是一种同质现象,即使在一个人身上,记忆巩固和记忆提取的障碍也可能由同一事件引起。动物研究总体上证实了这些结论。为了研究垂体肽对健忘症的影响,我们建立了一个动物模型。这个模型是基于二氧化碳诱导的健忘症对大鼠的一次试验被动回避反应。这种健忘症可以在检索试验前1小时用acth类似物治疗而减轻。acth类似物的抗健忘症作用不依赖于行为反应的性质或健忘症治疗。在检索试验前注射抗利尿激素类似物DGLVP同样具有抗遗忘作用。然而,与acth类似物相比,在获得前注射它也能减少健忘症。这些结果表明,健忘症可能包括“错误巩固”和“错误检索”成分,这可能由不同的垂体激素修正。因此,对多肽抗健忘症活性的研究不仅有助于表征这些多肽的行为效应的性质,而且可能被证明有助于揭示健忘症的过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pituitary hormones and amnesia.

Pituitary hormones profoundly influence behavior through direct actions on the brain. One of these behavioral effects is the attenuation of experimental amnesia. Traditionally, amnesia is considered as a "loss of memory." Memory comprises at least 2 stages: input (memory consolidation) and output (memory retrieval). Theoretically, disturbance of either aspect of memory may be the cause of amnesia. Also, it is possible that amnesia is based on a factor or factors not related to memory. Data and theories on amnesia in man were reviewed. Some salient features were mentioned: (1) amnesia can be induced by a variety of agents; (2) amnesia covers periods ranging from seconds to years; (3) amnesia gradients can be established; (4) amnesia is to a large extent reversible. From this survey, it seems possible that amnesia is not a homogeneous phenomenon and that even in one person a disturbance of both memory consolidation and memory retrieval may be produced by one and the same event. Animal studies in general have confirmed these conclusions. We have developed an animal model in order to study the effects of pituitary peptides on amnesia. This model is based on CO2-induced amnesia for a one-trial passive avoidance response in rats. This amnesia could be attenuated by treatment with ACTH-analogs 1 hour before the retrieval test. This anti-amnesic effect of ACTH-analogs was not dependent on the nature of the behavioral response or the amnesic treatment. The vasopressin-analog DGLVP similarly exerted an anti-amnesic effect when injected before the retrieval trial. In contrast to ACTH-analogs, however, it also reduced the amnesia when injected before acquisition. These results suggest that amnesia may comprise a "faulty-consolidation" and a "faulty-retrieval" component, which may be amended by different pituitary hormones. The study of the anti-amnesic activity of peptides therefore not only serves to characterize the nature of the behavioral effect of these peptides but may also prove to be helpful of the unraveling of processes involved in amnesia.

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