The disconnection hypothesis
The disconnection hypothesis
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DOI：
10.1016/s0920-9964(97)00140-0
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发表时间：
1998-03-10
影响因子：
4.5
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，并提出了一个机制的帐户，如何功能失调的神经系统之间的整合可能会出现。这种神经生物学的解释是基于神经元可塑性在塑造连接和随后的大脑功能动力学中所起的核心作用。这里提出的特殊假设是，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制水平上;特别是在产后时期负责情绪学习和记忆的大脑系统中的可塑性调制。这种调节是由上升的神经递质系统介导的，这些神经递质系统：（i）与精神分裂症有关;（ii）已知参与学习期间巩固突触连接。拟议的病理生理学将翻译，在功能方面，到一个中断的强化适应性行为，这是一致的分裂精神分裂症神经心理学方面。(C)1998年Elsevier Science B.V.
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. (C) 1998 Elsevier Science B.V.