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Phenomenology and classification of dystonia: a consensus update.特发性运动障碍的现象学和分类:共识更新。
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Dopamine D1, D2, D3 receptors, vesicular monoamine transporter type-2 (VMAT2) and dopamine transporter (DAT) densities in aged human brain.老年人大脑中的多巴胺 D1、D2、D3 受体、囊泡单胺转运体 2(VMAT2)和多巴胺转运体(DAT)密度。
PLoS One. 2012;7(11):e49483. doi: 10.1371/journal.pone.0049483. Epub 2012 Nov 21.
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Synthesis and evaluation of in vitro bioactivity for vesicular acetylcholine transporter inhibitors containing two carbonyl groups.含有两个羰基的囊泡型乙酰胆碱转运体抑制剂的合成与体外生物活性评价。
Bioorg Med Chem. 2012 Jul 15;20(14):4422-9. doi: 10.1016/j.bmc.2012.05.045. Epub 2012 May 30.
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Cholinergic dysregulation produced by selective inactivation of the dystonia-associated protein torsinA.选择性失活与肌张力障碍相关蛋白 torsinA 引起的胆碱能调节紊乱。
Neurobiol Dis. 2012 Sep;47(3):416-27. doi: 10.1016/j.nbd.2012.04.015. Epub 2012 May 3.
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Characterization of extrastriatal D2 in vivo specific binding of [¹⁸F](N-methyl)benperidol using PET.使用正电子发射断层扫描术(PET)对 [¹⁸F](N-甲基)苯丙哌醇在外周多巴胺 D2 进行体内特异性结合的特征描述。
Synapse. 2012 Sep;66(9):770-80. doi: 10.1002/syn.21566. Epub 2012 May 15.
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Alteration of striatal dopaminergic neurotransmission in a mouse model of DYT11 myoclonus-dystonia.DYT11 肌阵挛-肌张力障碍小鼠模型纹状体内多巴胺能神经传递的改变。
PLoS One. 2012;7(3):e33669. doi: 10.1371/journal.pone.0033669. Epub 2012 Mar 16.
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Diagnosis of dystonic syndromes--a new eight-question approach.诊断肌张力障碍综合征的新八问法。
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An anticholinergic reverses motor control and corticostriatal LTD deficits in Dyt1 ΔGAG knock-in mice.抗胆碱能药物可逆转 Dyt1 ΔGAG 敲入小鼠的运动控制和皮质纹状体 LTD 缺陷。
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Decreased striatal dopamine receptor binding in primary focal dystonia: a D2 or D3 defect?原发性局灶性肌张力障碍患者纹状体多巴胺受体结合减少:是 D2 还是 D3 缺陷?
Mov Disord. 2011 Jan;26(1):100-6. doi: 10.1002/mds.23401. Epub 2010 Oct 19.
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Imaging dopamine receptors in humans with [11C]-(+)-PHNO: dissection of D3 signal and anatomy.用 [11C]-(+)-PHNO 对人类多巴胺受体进行成像:D3 信号与解剖结构的剖析。
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纹状体多巴胺 D1 样受体结合在原发性局灶性肌张力障碍中保持不变。

Striatal dopamine D1-like receptor binding is unchanged in primary focal dystonia.

机构信息

Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri, USA.

出版信息

Mov Disord. 2013 Dec;28(14):2002-6. doi: 10.1002/mds.25720. Epub 2013 Oct 21.

DOI:10.1002/mds.25720
PMID:24151192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4086787/
Abstract

BACKGROUND

Multiple studies have demonstrated decreases in striatal D2-like (D2, D3) radioligand binding in primary focal dystonias. Although most investigations have focused on D2-specific receptors (D2R), a recent study suggests that the decreased D2-like binding may be due to a D3-specific (D3R) abnormality. However, only limited data exist on the role of D1-specific receptors (D1R) and the D1R-mediated pathways within basal ganglia in dystonia. Metabolic positron emission tomography (PET) data in primary generalized dystonia suggest resting state over activity in the D1R-mediated direct pathway, leading to excessive disinhibition of motor cortical areas. This work investigated whether striatal D1-like receptors are affected in primary focal dystonias.

METHODS

Striatal-specific (caudate and putamen) binding of the D1-like radioligand [(11)C]NNC 112 was measured using PET in 19 patients with primary focal dystonia (cranial, cervical, or arm) and 18 controls.

RESULTS

No statistically significant difference was detected in striatal D1-like binding between the two groups. The study had 91% power to detect a 20% difference, indicating that false-negative results were unlikely.

CONCLUSIONS

Because [(11)C]NNC 112 has high affinity for D1-like receptors, very low affinity for D2-like receptors, and minimal sensitivity to endogenous dopamine levels, we conclude that D1-like receptor binding is not impaired in these primary focal dystonias.

摘要

背景

多项研究表明,原发性局灶性肌张力障碍患者纹状体中 D2 样(D2、D3)放射性配体结合减少。尽管大多数研究都集中在 D2 特异性受体(D2R)上,但最近的一项研究表明,减少的 D2 样结合可能是由于 D3 特异性(D3R)异常。然而,关于 D1 特异性受体(D1R)和基底神经节中 D1R 介导的途径在肌张力障碍中的作用,仅有有限的数据。原发性全身性肌张力障碍的代谢正电子发射断层扫描(PET)数据表明,D1R 介导的直接途径中存在静息状态过度活动,导致运动皮质区域过度抑制。这项工作研究了原发性局灶性肌张力障碍中纹状体 D1 样受体是否受到影响。

方法

使用 PET 测量 19 例原发性局灶性肌张力障碍(颅、颈或臂)患者和 18 例对照者纹状体特异性(尾状核和壳核)D1 样放射性配体[11C]NNC 112 的结合。

结果

两组间纹状体 D1 样结合无统计学差异。该研究有 91%的效能检测到 20%的差异,表明假阴性结果不太可能。

结论

由于[11C]NNC 112 对 D1 样受体具有高亲和力,对 D2 样受体具有低亲和力,对内源性多巴胺水平的敏感性最小,我们得出结论,这些原发性局灶性肌张力障碍中 D1 样受体结合没有受损。