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深部脑刺激改变僵硬仓鼠基底神经节输出核的放电模式。

Deep brain stimulation changes basal ganglia output nuclei firing pattern in the dystonic hamster.

机构信息

CNRS UMR 5227, Université Victor Ségalen, Bordeaux, France.

出版信息

Neurobiol Dis. 2010 May;38(2):288-98. doi: 10.1016/j.nbd.2010.01.020. Epub 2010 Feb 4.

Abstract

Dystonia is a heterogeneous syndrome of movement disorders characterized by involuntary muscle contractions leading to abnormal movements and postures. While medical treatment is often ineffective, deep brain stimulation (DBS) of the internal pallidum improves dystonia. Here, we studied the impact of DBS in the entopeduncular nucleus (EP), the rodent equivalent of the human globus pallidus internus, on basal ganglia output in the dt(sz)-hamster, a well-characterized model of dystonia by extracellular recordings. Previous work has shown that EP-DBS improves dystonic symptoms in dt(sz)-hamsters. We report that EP-DBS changes firing pattern in the EP, most neurons switching to a less regular firing pattern during DBS. In contrast, EP-DBS did not change the average firing rate of EP neurons. EP neurons display multiphasic responses to each stimulation impulse, likely underlying the disruption of their firing rhythm. Finally, neurons in the substantia nigra pars reticulata display similar responses to EP-DBS, supporting the idea that EP-DBS affects basal ganglia output activity through the activation of common afferent fibers.

摘要

肌张力障碍是一种运动障碍的异质综合征,其特征是不自主的肌肉收缩导致异常运动和姿势。虽然药物治疗通常无效,但深部脑刺激(DBS)对苍白球内侧的改善作用。在这里,我们通过细胞外记录研究了内苍白球(EP),即人类苍白球内侧的啮齿动物对应物,在 dt(sz)-仓鼠中的基底神经节输出的影响,dt(sz)-仓鼠是一种经过充分特征描述的肌张力障碍模型。以前的工作表明,EP-DBS 可改善 dt(sz)-仓鼠的肌张力障碍症状。我们报告说,EP-DBS 改变了 EP 中的放电模式,大多数神经元在 DBS 期间切换到更不规则的放电模式。相比之下,EP-DBS 并未改变 EP 神经元的平均放电率。EP 神经元对每个刺激脉冲显示出多相反应,可能是其放电节律中断的基础。最后,黑质网状部的神经元对 EP-DBS 也有类似的反应,支持通过激活共同传入纤维来影响基底神经节输出活动的观点。

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