Ramírez-López Fernanda, García-Montes José Rubén, Millán-Aldaco Diana, Palomero-Rivero Marcela, Túnez-Fiñana Isaac, Drucker-Colín René, Roldán-Roldán Gabriel
Departamento de Neuropatología Molecular, Instituo de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.
Instituto Cajal, 28002 Madrid, Spain.
Brain Sci. 2024 Nov 29;14(12):1214. doi: 10.3390/brainsci14121214.
BACKGROUND/OBJECTIVES: Dopamine replacement therapy for Parkinson's disease (PD) may lead to disabling incontrollable movements known as L-DOPA-induced dyskinesias. Transcranial magnetic stimulation (TMS) has been applied as non-invasive therapy to ameliorate motor symptoms and dyskinesias in PD treatment. Recent studies have shown that TMS-induced motor effects might be related to dopaminergic system modulation. However, the mechanisms underlying these effects of TMS are not fully understood.
To assess the expression of FosB and c-Fos in dopamine-D1 receptor-containing cells of dyskinetic rats and to analyze the effect of TMS on dyskinetic behavior and its histological marker (FosB).
We investigated the outcome of TMS on cellular activation, using c-Fos immunoreactivity, on D1 receptor-positive (D1R+) cells into the motor cortex and striatum of dyskinetic ( = 14) and intact rats ( = 14). Additionally, we evaluated the effect of TMS on the dyskinesia global score and its molecular marker, FosB, in the striatum ( = 67).
TMS reduces c-Fos expression in D1R+cells into the motor cortex and striatum. Moreover, TMS treatment attenuated dyskinesias, along with a low stratal FosB expression.
The current study shows that TMS depressed FosB and c-Fos expression in D1R+ cells of the dorsal striatum and motor cortex, in accordance with previous evidence of its capacity to modulate the dopaminergic system, thus suggesting a mechanism by which TMS may mitigate dyskinesias. Additionally, our observations highlight the potential therapeutic effect of TMS on dyskinesias in a PD model.
背景/目的：帕金森病（PD）的多巴胺替代疗法可能会导致出现称为左旋多巴诱导的运动障碍的致残性无法控制的运动。经颅磁刺激（TMS）已被用作一种非侵入性疗法，以改善PD治疗中的运动症状和运动障碍。最近的研究表明，TMS诱导的运动效应可能与多巴胺能系统调节有关。然而，TMS这些效应的潜在机制尚未完全了解。
评估异动症大鼠含多巴胺D1受体细胞中FosB和c-Fos的表达，并分析TMS对异动行为及其组织学标志物（FosB）的影响。
我们使用c-Fos免疫反应性研究了TMS对异动症（n = 14）和正常大鼠（n = 14）运动皮层和纹状体中D1受体阳性（D1R+）细胞的细胞激活的影响。此外，我们评估了TMS对纹状体（n = 67）中异动症总体评分及其分子标志物FosB的影响。
TMS降低了运动皮层和纹状体中D1R+细胞中的c-Fos表达。此外，TMS治疗减轻了异动症，同时纹状体FosB表达降低。
当前研究表明，TMS降低了背侧纹状体和运动皮层D1R+细胞中FosB和c-Fos的表达，这与之前其调节多巴胺能系统能力的证据一致，从而提示了一种TMS可能减轻异动症的机制。此外，我们的观察结果突出了TMS对PD模型中异动症的潜在治疗作用。
