Cerebellar Contributions to Hypokinetic Symptoms in an Acute Lesion Parkinsonism Model.

IF 3.2 Q2 CLINICAL NEUROLOGY
Cristofer Zarate-Calderon, Gerardo Marín, Iraís Viveros-Martínez, Lizbeth Vásquez-Celaya, Porfirio Carrillo-Castilla, Gonzalo E Aranda-Abreu, Donaji Chi-Castañeda, Luis I García
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Abstract

Background: Parkinsonism, characterized by motor symptoms, is typically attributed to basal ganglia dysfunction. Recent evidence suggests that the cerebellum may also influence these symptoms. This study investigated Crus II, the dentate nucleus (DN), and the inferior olive (IO) in a rat model of parkinsonism induced by a bilateral ventrolateral striatal (VLS) lesion. Materials and Methods: Twenty-four male Wistar rats were divided into control (n = 12) and experimental (n = 12) groups. Monopolar electrodes were implanted in target structures. The experimental group received a bilateral VLS lesion. Animals underwent four weekly sessions of electrophysiological recordings and blind behavioral assessments (resting, grooming, locomotion, rearing, sniffing) via video tracking. Power spectral density (PSD) in the 300-500 Hz band was computed. Statistical analyses included Mann-Whitney U, Friedman with Wilcoxon post hoc, and Spearman correlation tests. Results: During weeks one and two, there were significant PSD increases in the experimental group compared to the control, particularly in Crus II-grooming (p = 0.005), locomotion (p = 0.007), and rearing (p = 0.026); in IO-sniffing (p = 0.0167); and in DN-grooming (p < 0.001) and locomotion (p = 0.0008). Additionally, intragroup analysis revealed significant PSD elevations relative to baseline in these structures. Significant correlations were observed only for grooming (negative correlations) and sniffing (positive correlations) across all cerebellar regions. Conclusions: These findings suggest compensatory cerebellar hyperactivity induced by VLS lesion, potentially modulating hypokinetic symptoms and highlighting dynamic network interactions. Interpretation warrants caution due to limitations inherent to the acute lesion model and experimental duration.

急性损伤性帕金森模型中小脑对运动障碍症状的影响
背景:帕金森病以运动症状为特征,通常归因于基底节区功能障碍。最近的证据表明,小脑也可能影响这些症状。本研究研究了双侧腹外侧纹状体(VLS)损伤引起的帕金森大鼠模型的II足、齿状核(DN)和下橄榄(IO)。材料与方法:24只雄性Wistar大鼠分为对照组(n = 12)和试验组(n = 12)。将单极电极植入目标结构。实验组采用双侧VLS病变。通过视频跟踪,动物每周进行四次电生理记录和盲目行为评估(休息、梳理、运动、饲养、嗅探)。计算了300 ~ 500 Hz频段的功率谱密度(PSD)。统计分析包括Mann-Whitney U、Friedman with Wilcoxon事后检验和Spearman相关检验。结果:与对照组相比,在第1周和第2周,实验组的PSD显著增加,特别是在ii号小腿-梳理(p = 0.005),运动(p = 0.007)和饲养(p = 0.026);io嗅探(p = 0.0167);梳毛(p < 0.001)和运动(p = 0.0008)。此外,组内分析显示,这些结构的PSD相对于基线有显著升高。在所有小脑区域中,只有梳理(负相关)和嗅探(正相关)观察到显著的相关性。结论:这些发现提示VLS病变引起的代偿性小脑亢进,可能调节运动不足症状并突出动态网络的相互作用。由于急性损伤模型和实验时间固有的局限性,解释需要谨慎。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neurology International
Neurology International CLINICAL NEUROLOGY-
CiteScore
3.70
自引率
3.30%
发文量
69
审稿时长
11 weeks
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