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胼胝体难题:通过神经网络模型在半球竞争背景下解释交叉性神经机能联系障碍

The callosal dilemma: explaining diaschisis in the context of hemispheric rivalry via a neural network model.

作者信息

Reggia J A, Goodall S M, Shkuro Y, Glezer M

机构信息

Department of Computer Science, Institute of Advanced Computer Studies, A.V. Williams Bldg., University of Maryland, College Park, MD 20742, USA.

出版信息

Neurol Res. 2001 Jul;23(5):465-71. doi: 10.1179/016164101101198857.

DOI:10.1179/016164101101198857
PMID:11474802
Abstract

It is often suggested that a major factor in diaschisis is the loss of transcallosal excitation to the intact hemisphere from the lesioned one. However, there is long-standing disagreement in the broader experimental literature about whether transcallosal interhemispheric influences in the human brain are primarily excitatory or inhibitory. Some experimental data are apparently better explained by assuming inhibitory callosal influences. Past neural network models attempting to explore this issue have encountered the same dilemma: in intact models, inhibitory callosal influences best explain strong cerebral lateralization like that occurring with language, but in lesioned models, excitatory callosal influences best explain experimentally observed hemispheric activation patterns following brain damage. We have now developed a single neural network model that can account for both types of data, i.e., both diaschisis and strong hemisphere specialization in the normal brain, by combining excitatory callosal influences with subcortical cross-midline inhibitory interactions. The results suggest that subcortical competitive processes may be a more important factor in cerebral specialization than is generally recognized.

摘要

人们常认为,失联络现象的一个主要因素是受损半球对完整半球的胼胝体间兴奋丧失。然而,在更广泛的实验文献中,关于人类大脑中胼胝体间半球影响主要是兴奋性还是抑制性,长期存在分歧。一些实验数据通过假设胼胝体抑制性影响似乎能得到更好的解释。过去试图探索这个问题的神经网络模型也遇到了同样的困境:在完整模型中,胼胝体抑制性影响最能解释像语言所发生的那种强烈的大脑半球侧化,但在受损模型中,胼胝体兴奋性影响最能解释脑损伤后实验观察到的半球激活模式。我们现在开发了一个单一的神经网络模型,通过将胼胝体兴奋性影响与皮质下跨中线抑制性相互作用相结合,能够解释这两种类型的数据,即失联络现象和正常大脑中强烈的半球特化。结果表明,皮质下竞争过程可能是大脑特化中比普遍认为的更重要的因素。

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