Rigter H, Van Riezen H
Curr Dev Psychopharmacol. 1979;5:67-124.
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.
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失忆的减轻。传统上，失忆被视为“记忆丧失”。记忆至少包括两个阶段：输入（记忆巩固）和输出（记忆检索）。理论上，记忆任何一个方面的干扰都可能是失忆的原因。此外，失忆也有可能基于与记忆无关的一个或多个因素。对人类失忆的数据和理论进行了综述。提到了一些显著特征：（1）失忆可由多种因素诱发；（2）失忆涵盖从数秒到数年的时间段；（3）可建立失忆梯度；（4）失忆在很大程度上是可逆的。从这项调查来看，失忆似乎不是一种单一的现象，而且即使在一个人身上，同一事件也可能导致记忆巩固和记忆检索都受到干扰。一般来说，动物研究证实了这些结论。我们开发了一种动物模型，以研究垂体肽对失忆的影响。该模型基于大鼠单次被动回避反应中二氧化碳诱导的失忆。在检索测试前1小时用促肾上腺皮质激素类似物治疗可减轻这种失忆。促肾上腺皮质激素类似物的这种抗失忆作用不依赖于行为反应的性质或失忆治疗方法。血管加压素类似物DGLVP在检索试验前注射时同样发挥了抗失忆作用。然而，与促肾上腺皮质激素类似物不同的是，它在习得前注射时也能减轻失忆。这些结果表明，失忆可能包括“巩固缺陷”和“检索缺陷”成分，不同的垂体激素可能对其进行修正。因此，对肽类抗失忆活性的研究不仅有助于表征这些肽类行为效应的性质，而且可能有助于揭示失忆所涉及的过程。
