Friston K J
Wellcome Department of Cognitive Neurology, Institute of Neurology, Queen Square, London, UK.
Schizophr Res. 1998 Mar 10;30(2):115-25. doi: 10.1016/s0920-9964(97)00140-0.
This article reviews the disconnection hypothesis of schizophrenia and presents a mechanistic account of how dysfunctional integration among neuronal systems might arise. This neurobiological account is based on the central role played by neuronal plasticity in shaping the connections and the ensuing dynamics that underlie brain function. The particular hypothesis put forward here is that the pathophysiology of schizophrenia is expressed at the level of modulation of associative changes in synaptic efficacy; specifically the modulation of plasticity in those brain systems responsible for emotional learning and memory, in the post-natal period. This modulation is mediated by ascending neurotransmitter systems that: (i) have been implicated in schizophrenia; and (ii) are known to be involved in consolidating synaptic connections during learning. The proposed pathophysiology would translate, in functional terms, into a disruption of the reinforcement of adaptive behaviour that is consistent with the disintegrative aspects of schizophrenic neuropsychology.
本文回顾了精神分裂症的脱节假说，并对神经元系统间功能失调的整合可能如何产生给出了一个机制性解释。这种神经生物学解释基于神经元可塑性在塑造连接以及构成脑功能基础的后续动态过程中所起的核心作用。这里提出的特定假说是，精神分裂症的病理生理学表现在突触效能的关联性变化调节水平；具体而言，是在出生后负责情绪学习和记忆的脑系统中可塑性的调节。这种调节由上行神经递质系统介导，这些系统：（i）与精神分裂症有关；（ii）已知在学习过程中参与巩固突触连接。从功能角度来看，所提出的病理生理学将转化为适应性行为强化的破坏，这与精神分裂症神经心理学的解体方面是一致的。
