Negative schizophrenic symptomatology and the PCP (phencyclidine) model of schizophrenia.
Negative schizophrenic symptomatology and the PCP (phencyclidine) model of schizophrenia.
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发表时间：
1987
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通讯作者：
D. Javitt
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作者：
D. Javitt
在过去的30年里，安非他命诱发的精神病为精神分裂症的研究提供了一个有用的模型。然而，安非他明模型已被证明有许多缺点，包括无法模拟精神分裂症的缺陷症状。PCP（苯环利定）已被证明能够诱导由生产和缺陷症状组成的精神分裂症样精神病。因此，PCP诱发的精神病可能为精神分裂症提供了一个有用的模型。本文综述了有关精神分裂症PCP模型的文献，并对PCP调节中脑皮层多巴胺能活性的能力提供了一些独立的证实。由于PCP似乎通过谷氨酸受体亚类介导其中枢神经系统作用，因此提出了一种可能的精神分裂症谷氨酸理论。
Amphetamine induced psychosis has for the past 30 years provided a useful model for the study of schizophrenia. The amphetamine model, however, has been shown to have a number of shortcomings including an inability to model the deficit symptoms of schizophrenia. PCP (phencyclidine) has been shown to be capable of inducing a schizophreniform psychosis consisting of both productive and defict symptomatology. PCP induced psychosis, therefore, may provide a useful model of schizophrenia. This paper reviews the literature concerning the PCP model of schizophrenia and provides some independent confirmation of the ability of PCP to modulate mesocortical dopaminergic activity. Since PCP appears to mediate its CNS effects via a subclass of glutamate receptors, a possible glutamate theory of schizophrenia is proposed.