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Association between striatal dopamine D2/D3 receptors andbrain activation during visual attention: effects of sleep deprivation

机译:纹状体多巴胺D2 / D3受体与视觉注意期间的大脑激活:睡眠剥夺的影响

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摘要

Sleep deprivation (SD) disrupts dopamine (DA) signaling and impairs attention. However, the interpretation of these concomitant effects requires a better understanding of dopamine’s role in attention processing. Here we test the hypotheses that D2/D3 receptors (D2/D3R) in dorsal and ventral striatum would distinctly regulate the activation of attention regions and that, by decreasing D2/D3, SD would disrupt these associations. We measured striatal D2/D3R using positron emission tomography with [11C]raclopride and brain activation to a visual attention (VA) task using 4-Tesla functional magnetic resonance imaging. Fourteen healthy men were studied during rested wakefulness and also during SD. Increased D2/D3R in striatum (caudate, putamen and ventral striatum) were linearly associated with higher thalamic activation. Subjects with higher D2/D3R in caudate relative to ventral striatum had higher activation in superior parietal cortex and ventral precuneus, and those with higher D2/D3R in putamen relative to ventral striatum had higher activation in anterior cingulate. SD impaired the association between striatalD2/D3R and VA-induced thalamic activation, which isessential for alertness. Findings suggest a robust DAergic modulation of corticalactivation during the VA task, such that D2/D3R in dorsalstriatum counterbalanced the stimulatory influence ofD2/D3R in ventral striatum, which was not significantlydisrupted by SD. In contrast, SD disrupted thalamic activation, which did not showcounterbalanced DAergic modulation but a positive association withD2/D3R in both dorsal and ventral striatum. Thecounterbalanced dorsal versus ventral striatal DAergic modulation of VA activationmirrors similar findings during sensorimotor processing (Tomasi et al.,2015) suggesting a bidirectional influence in signaling between the dorsal caudateand putamen and the ventral striatum.
机译:睡眠剥夺(SD)会破坏多巴胺(DA)信号传导并损害注意力。但是,对这些伴随效应的解释要求更好地了解多巴胺在注意力加工中的作用。在这里,我们测试了以下假设:背侧和腹侧纹状体中的D2 / D3受体(D2 / D3R)将明显调节注意力区域的激活,并且通过降低D2 / D3,SD将破坏这些关联。我们使用正电子发射断层显像和[ 11 C]雷氯必利测量脑纹状体D2 / D3R,并使用4-Tesla功能磁共振成像将大脑激活至视觉注意力(VA)任务。在休息的清醒期间以及在SD期间对14名健康男性进行了研究。纹状体(尾状,壳状核和腹侧纹状体)中D2 / D3R的增加与较高的丘脑激活呈线性关系。相对于腹侧纹状体,尾状D2 / D3R较高的受试者在上顶皮层和腹前神经中具有较高的活化,而相对于腹侧纹状体,壳状蛋白的D2 / D3R较高的受试者在前扣带中具有较高的活化。 SD损害纹状体之间的关联D2 / D3R和VA诱导的丘脑激活,这是保持警惕至关重要。研究结果表明皮质的强大DA能量调制在VA任务期间激活,使得背侧的D 2 / D 3 R纹状体抵消了刺激的影响腹侧纹状体中的D 2 / D 3 R受SD干扰。相反,SD破坏了丘脑的激活,但并未显示抗衡DA能量调制,但与背侧和腹侧纹状体中的D 2 / D 3 R。的背侧和腹侧纹状体对VA激活的平衡调节反映了感觉运动过程中的类似发现(Tomasi等,2015)暗示了在尾背之间的信号传递的双向影响以及壳核和腹侧纹状体。

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