Inactivation of the parietal reach region causes optic ataxia, impairing reaches but not saccades.

Inactivation of the parietal reach region causes optic ataxia, impairing reaches but not saccades.
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DOI:
10.1016/j.neuron.2012.10.030
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发表时间:
2012-12-06
期刊:
影响因子:
16.2
通讯作者:
Andersen RA
Andersen RA
中科院分区:
医学1区
文献类型:
--
作者:
Hwang EJ;Hauschild M;Wilke M;Andersen RA

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人类后顶叶皮层的病变可导致视共济失调(OA),其中对视觉对象的到达而不是扫视受损,这表明两种效应器的视觉通路是分开的。在猴子中,达到控制的一个潜在的关键领域是顶叶达到区域(PRR),其中神经元优先响应达到规划相比,扫视规划。然而,缺乏将猴PRR与OA中观察到的缺陷联系起来的直接因果证据。因此,我们灭活了猕猴PRR的一部分,在顶内沟的内侧壁,并产生了OA的标志,误触及外周目标,但未受损的扫视。此外,到达误差较大的注射部位的神经群体的首选目标。这些结果表明,PRR是因果关系参与达到特定的视觉通路,PRR中的达到目标中断可能是OA的神经基础。
Lesions in human posterior parietal cortex can cause optic ataxia (OA), in which reaches but not saccades to visual objects are impaired, suggesting separate visuomotor pathways for the two effectors. In monkeys, one potentially crucial area for reach control is the parietal reach region (PRR), in which neurons respond preferentially during reach planning as compared to saccade planning. However, direct causal evidence linking the monkey PRR to the deficits observed in OA is missing. We thus inactivated part of the macaque PRR, in the medial wall of the intraparietal sulcus, and produced the hallmarks of OA, misreaching for peripheral targets but unimpaired saccades. Furthermore, reach errors were larger for the targets preferred by the neural population local to the injection site. These results demonstrate that PRR is causally involved in reach-specific visuomotor pathways, and reach goal disruption in PRR can be a neural basis of OA.
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