Friston K J
Wellcome Department of Cognitive Neurology, Institute of Neurology, London, UK.
Acta Psychiatr Scand Suppl. 1999;395:68-79. doi: 10.1111/j.1600-0447.1999.tb05985.x.
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 some simple observations about schizophrenia and the central role that neuronal plasticity plays 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 that are responsible for learning, memory and emotion. 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一些关于精神分裂症的简单观察，以及神经元可塑性在塑造构成脑功能基础的连接及后续动态过程中所起的核心作用。这里提出的特定假说为，精神分裂症的病理生理学表现在突触效能联想性变化的调节层面，具体而言是那些负责学习、记忆和情感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。
