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未定带:在中枢性疼痛中的作用。

Zona incerta: a role in central pain.

作者信息

Masri Radi, Quiton Raimi L, Lucas Jessica M, Murray Peter D, Thompson Scott M, Keller Asaf

机构信息

Department of Anatomy, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD 21201, USA.

出版信息

J Neurophysiol. 2009 Jul;102(1):181-91. doi: 10.1152/jn.00152.2009. Epub 2009 Apr 29.

DOI:10.1152/jn.00152.2009
PMID:19403748
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2712264/
Abstract

Central pain syndrome (CPS) is a debilitating condition that affects a large number of patients with a primary lesion or dysfunction in the CNS. Despite its discovery over a century ago, the pathophysiological processes underlying the development and maintenance of CPS are poorly understood. We recently demonstrated that activity in the posterior thalamus (PO) is tightly regulated by inhibitory inputs from zona incerta (ZI). Here we test the hypothesis that CPS is associated with abnormal inhibitory regulation of PO by ZI. We recorded single units from ZI and PO in animals with CPS resulting from spinal cord lesions. Consistent with our hypothesis, the spontaneous firing rate and somatosensory evoked responses of ZI neurons were lower in lesioned animals compared with sham-operated controls. In PO, neurons recorded from lesioned rats exhibited significantly higher spontaneous firing rates and greater responses to noxious and innocuous stimuli applied to the hindpaw and to the face. These changes were not associated with increased afferent drive from the spinal trigeminal nucleus or changes in the ventroposterior thalamus. Thus CPS can result from suppressed inputs from the inhibitory nucleus zona incerta to the posterior thalamus.

摘要

中枢性疼痛综合征(CPS)是一种使人衰弱的病症,影响着大量中枢神经系统存在原发性损伤或功能障碍的患者。尽管它在一个多世纪前就已被发现,但对CPS发生和维持的病理生理过程仍知之甚少。我们最近证明,丘脑后部(PO)的活动受到未定带(ZI)抑制性输入的严格调控。在此,我们检验CPS与ZI对PO的异常抑制性调控相关这一假说。我们在因脊髓损伤导致CPS的动物中记录了ZI和PO的单个神经元活动。与我们的假说一致,与假手术对照组相比,损伤动物中ZI神经元的自发放电率和体感诱发电反应较低。在PO中,损伤大鼠记录到的神经元表现出自发放电率显著更高,并且对施加于后爪和面部的有害及无害刺激有更大反应。这些变化与来自脊髓三叉神经核的传入驱动增加或丘脑腹后核的变化无关。因此,CPS可能是由于抑制性核团未定带对丘脑后部的输入受到抑制所致。

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本文引用的文献

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Maladaptive homeostatic plasticity in a rodent model of central pain syndrome: thalamic hyperexcitability after spinothalamic tract lesions.中枢性疼痛综合征啮齿动物模型中的适应性不良稳态可塑性:脊髓丘脑束损伤后丘脑兴奋性过高
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