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MPTP 处理的猴子中丘脑中央中核的损伤。

Lesion of the centromedian thalamic nucleus in MPTP-treated monkeys.

作者信息

Lanciego Jose L, Rodríguez-Oroz Maria C, Blesa Francisco J, Alvarez-Erviti Lydia, Guridi Jorge, Barroso-Chinea Pedro, Smith Yoland, Obeso Jose A

机构信息

Neurosciences Division, CIMA, Pamplona, University of Navarra, Spain.

出版信息

Mov Disord. 2008 Apr 15;23(5):708-15. doi: 10.1002/mds.21906.

DOI:10.1002/mds.21906
PMID:18175345
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4413905/
Abstract

The caudal intralaminar nuclei are a major source of glutamatergic afferents to the basal ganglia. Experiments in the 6-hydroxydopamine rat model have shown that the parafascicular nucleus is overactive and its lesion alleviates basal ganglia neurochemical abnormalities associated with dopamine depletion. Accordingly, removal of this excitatory innervation of the basal ganglia could have a beneficial value in the parkinsonian state. To test this hypothesis, unilateral kainate-induced chemical ablation of the centromedian thalamic nucleus (CM) has been performed in MPTP-treated monkeys. Successful lesions restricted to the CM boundaries (n = 2) without spreading over other neighboring thalamic nuclei showed an initial, short-lasting, and mild change in the parkinsonian motor scale but no effect against levodopa-induced dyskinesias. The lack of significant and persistent motor improvement leads us to conclude that unilateral selective lesion of the CM alone cannot be considered as a suitable surgical approach for the treatment of PD or levodopa-induced dyskinesias. The role of the caudal intralaminar nuclei in the pathophysiology of movement disorders of basal ganglia origin remains to be clarified.

摘要

尾侧丘脑板内核是基底神经节谷氨酸能传入神经的主要来源。在6-羟基多巴胺大鼠模型中进行的实验表明,束旁核过度活跃,其损伤可减轻与多巴胺耗竭相关的基底神经节神经化学异常。因此,去除基底神经节的这种兴奋性神经支配可能对帕金森病状态具有有益价值。为了验证这一假设,在MPTP处理的猴子中进行了单侧海人酸诱导的中央中核(CM)化学毁损。成功的毁损局限于CM边界(n = 2),未扩散至其他相邻丘脑核,在帕金森运动量表上显示出最初的、短暂的、轻微的变化,但对左旋多巴诱导的异动症无效。缺乏显著且持续的运动改善使我们得出结论,仅单侧选择性毁损CM不能被视为治疗帕金森病或左旋多巴诱导的异动症的合适手术方法。尾侧丘脑板内核在基底神经节起源的运动障碍病理生理学中的作用仍有待阐明。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/89eed8f9b824/nihms-682708-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/122c160aa14f/nihms-682708-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/cdd163cfd72f/nihms-682708-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/3a088d815d03/nihms-682708-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/89eed8f9b824/nihms-682708-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/122c160aa14f/nihms-682708-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/cdd163cfd72f/nihms-682708-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/3a088d815d03/nihms-682708-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf3/4413905/89eed8f9b824/nihms-682708-f0004.jpg

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本文引用的文献

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Bilateral Implantation of Centromedian-Parafascicularis Complex and GPi: A New Combination of Unconventional Targets for Deep Brain Stimulation in Severe Parkinson Disease.丘脑中央中核-束旁核复合体与苍白球内侧部双侧植入:严重帕金森病脑深部电刺激的一种新的非传统靶点组合。
Neuromodulation. 2006 Jul;9(3):221-8. doi: 10.1111/j.1525-1403.2006.00063.x.
2
Deep brain stimulation in Tourette's syndrome.抽动秽语综合征的深部脑刺激疗法
Mov Disord. 2007 Jul 15;22(9):1346-50. doi: 10.1002/mds.21398.
3
Bilateral deep brain stimulation of the pedunculopontine and subthalamic nuclei in severe Parkinson's disease.双侧脑深部电刺激术治疗重度帕金森病的脚桥核与丘脑底核
Brain. 2007 Jun;130(Pt 6):1596-607. doi: 10.1093/brain/awl346. Epub 2007 Jan 24.
4
Circuits and circuit disorders of the basal ganglia.基底神经节的神经回路及其紊乱
Arch Neurol. 2007 Jan;64(1):20-4. doi: 10.1001/archneur.64.1.20.
5
Consequences of unilateral nigrostriatal denervation on the thalamostriatal pathway in rats.大鼠单侧黑质纹状体去神经支配对丘脑纹状体通路的影响。
Eur J Neurosci. 2006 Apr;23(8):2099-108. doi: 10.1111/j.1460-9568.2006.04741.x.
6
Deep brain stimulation in Tourette's syndrome: two targets?抽动秽语综合征中的深部脑刺激:两个靶点?
Mov Disord. 2006 May;21(5):709-13. doi: 10.1002/mds.20816.
7
Parafascicular nucleus projection to the extrastriatal basal ganglia in monkeys.猴子中束旁核向纹状体外基底神经节的投射。
Neuroreport. 2006 Feb 27;17(3):277-80. doi: 10.1097/01.wnr.0000201508.46126.de.
8
Behavioural effects of parafascicular thalamic lesions in an animal model of parkinsonism.帕金森病动物模型中束旁丘脑损伤的行为学效应
Behav Brain Res. 2005 Jul 30;162(2):222-32. doi: 10.1016/j.bbr.2005.03.017. Epub 2005 Apr 18.
9
Tourette's syndrome and deep brain stimulation.抽动秽语综合征与脑深部电刺激术
J Neurol Neurosurg Psychiatry. 2005 Jul;76(7):992-5. doi: 10.1136/jnnp.2004.043273.
10
Complementary process to response bias in the centromedian nucleus of the thalamus.丘脑中央中核反应偏差的互补过程。
Science. 2005 Jun 17;308(5729):1798-801. doi: 10.1126/science.1109154.