Corticocortical connectivity, autonomous networks, and schizophrenia.

Corticocortical connectivity, autonomous networks, and schizophrenia.
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皮质连接、自主网络和精神分裂症。

DOI:
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发表时间:
1994
影响因子:
6.6
通讯作者:
T. McGlashan
T. McGlashan
中科院分区:
医学1区
文献类型:
--
作者:
R. Hoffman;T. McGlashan

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大卫博士假设是皮质-皮质连接的增加而不是减少导致了精神分裂症。他引用了一些研究来支持他的假设,这些研究表明,这种疾病中存在过度的语义启动和跨半球干扰。大卫认为,这些发现反映了神经元之间或神经系统内部信息的过度传递。然而,在仅根据认知研究作出神经解剖学推论时,应相当谨慎。越来越多的人认为,信息是由大脑作为神经激活的模式来表现的,在这种模式下,同一个神经元或一组神经元参与了许多不同的表现。我们的模拟反映了这一共识,表明持久的或侵入性的激活模式不是来自太多的神经连接,而是来自太少的神经连接。这种情况导致神经元亚群忽略其他神经元的信息处理,而自主地产生自己的输出,这干扰了整个系统的功能。需要对大脑皮层进行直接的神经解剖学或神经化学研究,以充分评估有关精神分裂症中皮质连接异常的假设。
Dr. David hypothesizes that increased, not decreased, corticocortical connectivity causes schizophrenia. He cites studies suggesting excessive semantic priming and cross-hemispheric interference in this disorder to support his hypothesis. These findings, David suggests, reflect excessive transmission of information between neurons or within neural systems. However, considerable caution should be exercised in making neuroanatomic inferences on the basis of cognitive studies alone. There is an increasing consensus that information is represented by the brain as patterns of neural activation, where the same neuron or group of neurons participates in many different representations. Our simulations, which reflect this consensus, suggest that persistent or intrusive activation patterns do not emerge from too many neural connections, but from too few. This condition causes subgroups of neurons to disregard information processing by other neurons and to produce autonomously their own output, which interferes with the functioning of the system as a whole. Direct neuroanatomic or neurochemical studies of the cerebral cortex are needed to fully assess hypotheses regarding abnormal corticocortical connectivity in schizophrenia.
DOI: 10.1037/0033-295x.99.1.45
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发表时间: 1991
期刊: The Journal of neuropsychiatry and clinical neurosciences
影响因子: --
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