Zarate-Calderon Cristofer, Marín Gerardo, Viveros-Martínez Iraís, Vásquez-Celaya Lizbeth, Carrillo-Castilla Porfirio, Aranda-Abreu Gonzalo E, Chi-Castañeda Donaji, García Luis I
Instituto de Investigaciones Cerebrales, Universidad Veracruzana, Xalapa 91190, Mexico.
Departamento de Neurocirugía, "Hospital Regional 1° de Octubre", Instituto de Seguridad y Servicios Sociales de los Trabajadores del Estado, Mexico City 07300, Mexico.
Neurol Int. 2025 May 7;17(5):72. doi: 10.3390/neurolint17050072.
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. Twenty-four male rats were divided into control ( = 12) and experimental ( = 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. During weeks one and two, there were significant PSD increases in the experimental group compared to the control, particularly in Crus II-grooming ( = 0.005), locomotion ( = 0.007), and rearing ( = 0.026); in IO-sniffing ( = 0.0167); and in DN-grooming ( < 0.001) and locomotion ( = 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. 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.
帕金森综合征以运动症状为特征，通常归因于基底神经节功能障碍。最近的证据表明，小脑也可能影响这些症状。本研究在双侧腹外侧纹状体（VLS）损伤诱导的帕金森病大鼠模型中，对小脑 Crus II、齿状核（DN）和下橄榄核（IO）进行了研究。24只雄性大鼠分为对照组（n = 12）和实验组（n = 12）。将单极电极植入目标结构。实验组接受双侧VLS损伤。动物每周进行四次电生理记录，并通过视频跟踪进行盲法行为评估（静息、梳理、运动、竖毛、嗅探）。计算300 - 500 Hz频段的功率谱密度（PSD）。统计分析包括曼-惠特尼U检验、Friedman检验及Wilcoxon事后检验和斯皮尔曼相关性检验。在第1周和第2周，与对照组相比，实验组的PSD显著增加，特别是在Crus II - 梳理（P = 0.005）、运动（P = 0.007）和竖毛（P = 0.026）方面；在IO - 嗅探（P = 0.0167）方面；以及在DN - 梳理（P < 0.001）和运动（P = 0.0008）方面。此外，组内分析显示这些结构中相对于基线的PSD显著升高。仅在所有小脑区域的梳理（负相关）和嗅探（正相关）方面观察到显著相关性。这些发现表明VLS损伤诱导了小脑的代偿性多动，可能调节运动减少症状并突出了动态网络相互作用。由于急性损伤模型和实验持续时间固有的局限性，解释时需谨慎。
