Schizophrenia and the disconnection hypothesis
Schizophrenia and the disconnection hypothesis
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DOI：
10.1111/j.1600-0447.1999.tb05985.x
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发表时间：
1999-01-01
影响因子：
6.7
通讯作者：
Friston, KJ
中科院分区：
文献类型：
--
作者：
Friston, KJ
本文回顾了精神分裂症的断开假说，并提出了神经元系统之间整合功能失调如何可能出现的机制解释。这种神经生物学的解释是基于对精神分裂症的一些简单观察，以及神经元可塑性在塑造大脑功能基础的连接和随之而来的动态方面所发挥的核心作用。这里提出的具体假设是，精神分裂症的病理生理学表现在突触功效的关联变化的调节水平上，特别是负责学习、记忆和情感的大脑系统中可塑性的调节。这种调节是由上行神经递质系统介导的，该系统（i）与精神分裂症有关，（ii）已知参与巩固学习过程中的突触连接。从功能角度来说，所提出的病理生理学将转化为对适应性行为强化的破坏，这与精神分裂症神经心理学的瓦解方面是一致的。
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.