Inhibition of subliminally primed responses is mediated by the caudate and thalamus: evidence from functional MRI and Huntington's disease.

Inhibition of subliminally primed responses is mediated by the caudate and thalamus: evidence from functional MRI and Huntington's disease.
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尾状反应的抑制是由尾状和丘脑介导的:功能性MRI和亨廷顿氏病的证据。

DOI:
10.1093/brain/awg067
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发表时间:
2003-03
期刊:
Brain : a journal of neurology
影响因子:
--
通讯作者:
Robbins TW
Robbins TW
中科院分区:
其他
文献类型:
--
作者:
Aron AR;Schlaghecken F;Fletcher PC;Bullmore ET;Eimer M;Barker R;Sahakian BJ;Robbins TW

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掩蔽启动任务表明,没有被有意识感知的感觉信息仍然可以触发运动反应的预激活。自动抑制控制过程防止这种反应倾向干扰行为。本研究调查的可能性,这些抑制性控制过程是由皮质-纹状体-苍白球-丘脑通路介导的,通过使用一个掩蔽的主任务与亨廷顿病患者(实验1)和健康志愿者在功能性MRI(fMRI)研究(实验2)。在掩蔽启动任务中,清晰可见的指向左或右的目标箭头之前是简要呈现的,随后是掩蔽的启动箭头。参与者通过向左或向右按键快速响应每个目标。试模既可以兼容(预充和目标指向同一方向),也可以不兼容(预充和目标指向不同方向)。先前的行为学和电生理学结果表明,最初引发的反应倾向的自动抑制反映在“负相容性效应”中。(不相容试验的反应时间比相容试验的反应时间更快),并显示由三个不同的过程组成(主要激活,反应抑制和反应冲突)实验1通过研究纹状体损伤的早期--亨廷顿舞蹈病患者。调查结果支持这一假设:对于患者,存在双峰分布,其中三分之一(舞蹈病)显示去抑制,表现为不存在负相容性效应,并且三分之二(非舞蹈病)显示过度抑制,表现为比对照组显著更大的负相容性效应。实验2使用功能磁共振成像和感兴趣的区域(ROI)模板为基础的方法,以进一步测试的假设,纹状体-苍白球-丘脑通路的结构介导的一个或多个自动抑制控制的过程。无论是启动激活或反应冲突显着从事任何ROI,但反应抑制过程导致尾状核和丘脑的显着调制。两者合计,这些实验表明尾状核和丘脑在自动抑制运动控制中的因果作用,并且结果与需要直接和间接纹状体-苍白球丘脑通路的任务的性能是一致的。发现亨廷顿病患者的舞蹈症是解除抑制是一致的理论,舞蹈症产生的选择性变性的纹状体投射到外侧苍白球,而夸大的抑制效果,很少或没有舞蹈症的患者可能是由于额外的退化的投射到内侧苍白球。
Masked prime tasks have shown that sensory information that has not been consciously perceived can nevertheless trigger the preactivation of a motor response. Automatic inhibitory control processes prevent such response tendencies from interfering with behaviour. The present study investigated the possibility that these inhibitory control processes are mediated by a cortico-striatal-pallidal-thalamic pathway by using a masked prime task with Huntington’s disease patients (Experiment 1) and with healthy volunteers in a functional MRI (fMRI) study (Experiment 2). In the masked prime task, clearly visible left- or right-pointing target arrows are preceded by briefly presented and subsequently masked prime arrows. Participants respond quickly with a left or right key-press to each target. Trials are either compatible (prime and target pointing in the same direction) or incompatible (prime and target pointing in different directions). Prior behavioural and electrophysiological results show that automatic inhibition of the initially primed response tendency is reflected in a ‘negative compatibility effect’ (faster reaction times for incompatible trials than for compatible trials), and is shown to consist of three distinct processes (prime activation, response inhibition and response conflict) occurring within 300 ms. Experiment 1 tested the hypothesis that lesions of the striatum would interrupt automatic inhibitory control by studying early-stage Huntington’s disease patients. Findings supported the hypothesis: there was a bimodal distribution for patients, with one-third (choreic) showing disinhibition, manifested as an absent negative compatibility effect, and two-thirds (non-choreic) showing excessive inhibition, manifested as a significantly greater negative compatibility effect than that in controls. Experiment 2 used fMRI and a region of interest (ROI) template-based method to further test the hypothesis that structures of the striatal-pallidal-thalamic pathway mediate one or more of the processes of automatic inhibitory control. Neither prime activation nor response conflict significantly engaged any ROIs, but the response inhibition process led to significant modulation of both the caudate and thalamus. Taken together, these experiments indicate a causal role for the caudate nucleus and thalamus in automatic inhibitory motor control, and the results are consistent with performance of the task requiring both direct and indirect striatal-pallidalthalamic pathways. The finding that Huntington’s disease patients with greater chorea were disinhibited is consistent with the theory that chorea arises from selective degeneration of striatal projections to the lateral globus pallidus, while the exaggerated inhibitory effect for patients with little or no chorea may be due to additional degeneration of projections to the medial globus pallidus.
DOI: 10.1212/wnl.37.3.364
发表时间: 1987-03-01
期刊: NEUROLOGY
影响因子: 9.9
作者:
LASKER, AG;ZEE, DS;SINGER, HS
通讯作者: SINGER, HS
DOI: 10.1037/0096-1523.24.6.1737
发表时间: 1998-12-01
影响因子: 2.1
作者:
Eimer, M;Schlaghecken, F
通讯作者: Schlaghecken, F
DOI: 10.1037/0096-1523.14.3.331
发表时间: 1988-08-01
影响因子: 2.1
作者:
GRATTON, G;COLES, MGH;DONCHIN, E
通讯作者: DONCHIN, E
DOI: 10.3758/bf03212139
发表时间: 2000-10-01
期刊: PERCEPTION & PSYCHOPHYSICS
影响因子: --
作者:
Schlaghecken, F;Eimer, M
通讯作者: Eimer, M
DOI: 10.2466/pms.92.1.208-222
发表时间: 2001-02-01
影响因子: 1.6
作者:
Schlaghecken, F;Eimer, M
通讯作者: Eimer, M