Animal models with construct validity for schizophrenia.

Animal models with construct validity for schizophrenia.
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具有精神分裂症结构效度的动物模型。

DOI:
10.1097/00008877-199000160-00001
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发表时间:
1990
影响因子:
1.6
通讯作者:
A. Cools
A. Cools
中科院分区:
心理学4区
文献类型:
--
作者:
B. Ellenbroek;A. Cools

文献摘要

被引文献

相似文献

开发精神疾病的动物模型是一个复杂的过程。这主要是由于我们对抑郁症和精神分裂症等复杂疾病的基本过程的了解相对有限。不幸的是,这可能导致恶性循环。我们对这种疾病的有限知识导致无法开发适当的动物模型,这将导致无法增加我们对疾病背后的神经机制的知识。在本次审查中,我们试图表明,精神分裂症的情况正在慢慢改变。临床医师利用电生理学和心理学的方法,开始了解精神分裂症过程背后的精神病理过程。临床前研究人员试图利用这些知识来开发动物模型,在这些模型中可以测试假设,并可能深入了解疾病的潜在机制。在本综述中,提出了三种不同的动物模型。这些都是基于精神分裂症患者在他们的信息处理干扰的结构。更确切地说,前两个动物模型是基于精神分裂症患者不太能够区分相关和不相关刺激的结构。对文献的分析表明,安非他明引起的潜伏抑制(可能是阻断)的干扰,和苯环己哌啶引起的惊吓反应的干扰可能提供两个有趣的动物模型的结构,面子和预测效度的精神分裂症。第三个模型涉及安非他明引起的社会生活猴子行为变化。这个模型似乎与精神分裂症的阳性和阴性症状都有关,并且基于这样的结构,即阴性症状是由于保护受试者免受“感觉洪水”的补偿机制。安非他明引起的社会生活猴子行为变化似乎代表了一个动物模型的例子,其中既有阳性症状(刻板),也有阴性症状(社会孤立)。该模型的结构效度尚不清楚,但药理学研究表明,除了表面效度外,该模型还具有一定的预测效度。在本综述中讨论的模型可以帮助我们增加我们的洞察力的神经元结构的信息处理障碍。已知与这些模型有关的结构包括海马体、杏仁核和腹侧纹状体。
Developing animal models for psychiatric disorders is a complicated process. This is principally due to our relatively limited knowledge of the processes underlying such complicated illnesses as depression and schizophrenia. Unfortunately this can lead to a vicious circle. Our limited knowledge of the disease leads to the inability to develop proper animal models, which will lead to an inability to increase our knowledge about neuronal mechanisms underlying the illness. In the present review we have tried to show that with respect to schizophrenia the situation is slowly changing. Using electrophysiological and psychological methods, clinicians begin to understand the psychopathological processes underlying the schizophrenic process. Preclinical researchers have tried to use this knowledge to develop animal models in which hypotheses can be tested and possible insight into mechanisms underlying the disease can be gained. In the present review three different animal models are presented. These are based on the construct that schizophrenic patients are disturbed in their information processing. More precisely the first two animal models are based on the construct that schizophrenic patients are less able to differentiate between relevant and irrelevant stimuli. The analysis of the literature suggests that the amphetamine-induced distruption of latent inhibition (and probably blocking), and the phencyclidine-induced disturbances in the startle response might provide two interesting animal models with construct, face and predictive validity for schizophrenia. This third model deals with the amphetamine-induced changes in the behaviour of socially living monkeys. This model seems to be related to both positive and negative symptoms of schizophrenia and is based on the construct that the negative symptoms are due to a compensatory mechanism which protects the subjects from "sensory flooding". The amphetamine-induced changes in behaviour of socially living monkeys seem to represent an example of an animal model in which both positive symptoms (stereotypy) and negative symptoms (social isolation) occurs. The construct validity of this model is still unclear, but pharmacological studies suggest that, apart from the face validity, the model also has a certain predictive validity. The models discussed in the present review can help us to increase our insight in neuronal structures underlying information processing disturbances. Structures known to be implicated in these models include the hippocampus, amygdala and ventral striatum.