Joseph M H, Frith C D, Waddington J L
Psychopharmacology (Berl). 1979 Jun 21;63(3):273-80. doi: 10.1007/BF00433561.
A hypothesis is briefly discussed proposing that schizophrenic symptoms are due to a breakdown in a mechanism by which conscious attention is limited and directed. It is shown that this mechanism can be modelled in terms of a simple nerve network in which every channel inhibits all the others. Failure of this inhibition would cause the defect hypothesised to occur in schizophrenia. It is shown that if dopamine is given a central role as transmitter in such a network then the various predictions about the biochemistry of schizophrenia that follow are not only consistent with the evidence for the 'dopamine theory' of schizophrenia, but also with much of the evidence held to be contrary to that theory. While not purporting to be an experimentally validated description of schizophrenia, this model goes beyond the single amine theories of schizophrenia and links dysfunctions in amine systems with specific behavioural control mechanisms. Given the current state of knowledge, such models can make only limited predictions about the biochemistry of schizophrenia. However, an attempt to link behavioural and biochemical systems in this way will be crucial for the development of viable animal models of schizophrenia.
本文简要讨论了一种假说，该假说认为精神分裂症症状是由于意识注意力受限和定向机制的崩溃所致。研究表明，这种机制可以用一个简单的神经网络来模拟，其中每个通道都会抑制其他所有通道。这种抑制作用的失败会导致精神分裂症中假设的缺陷出现。研究表明，如果多巴胺在这样一个网络中作为递质发挥核心作用，那么随后关于精神分裂症生物化学的各种预测不仅与精神分裂症“多巴胺理论”的证据一致，而且与许多被认为与该理论相悖的证据也一致。虽然本模型并非旨在成为对精神分裂症的实验验证描述，但它超越了精神分裂症的单胺理论，并将胺系统的功能障碍与特定的行为控制机制联系起来。鉴于目前的知识水平，此类模型只能对精神分裂症的生物化学做出有限的预测。然而，以这种方式将行为和生物化学系统联系起来的尝试对于开发可行的精神分裂症动物模型至关重要。
