Stepanyan Harutyun, Poghosyan Mikhail, Hovsepyan Maia, Sargsyan Rafik, Danielyan Margarita, Minasyan Arsen, Hunanyan Naira, Karapetyan Kristina, Sarkissian John
L. A. Orbeli Institute of Physiology, National Academy of Sciences of the Republic of Armenia, Yerevan, Armenia.
Department of Medical Biological Subjects, University of Traditional Medicine, Yerevan, Armenia.
Korean J Pain. 2025 Jul 1;38(3):282-291. doi: 10.3344/kjp.24385. Epub 2025 Jun 25.
The involvement of antinociceptive centers in neurodegeneration within the brain, particularly in Parkinson's disease (PD), which is accompanied by chronic pain, is not yet well understood.
Electrophysiological recordings were conducted on 15 king albino rats across three experimental conditions: intact, a rotenone-induced PD model, and a PD model treated with hydrocortisone. Extracellular spike activity was recorded from 241 single neurons in the periaqueductal gray (PAG) in response to stimulation of the raphe magnus nucleus (RMG).
The PD model exhibited significant excitotoxicity in the recorded neurons, indicative of substantial neurodegeneration, which appeared to precede both depressor (tetanic depression [TD], post-tetanic depression [PTD]) and excitatory (tetanic potentiation [TP], post-tetanic potentiation [PTP]) post-stimulus effects. A mathematical analysis of pre- and post-stimulus activation frequencies revealed the following: in the PD model with hydrocortisone protection, compared to the unprotected PD model, the pre-stimulus activation frequency of PAG neurons during high-frequency stimulation of the RMG was reduced, bringing the values closer to normal levels. The post-stimulus activation frequency of PAG neurons in the treatment group also decreased, both in depressor (TD, PTD) and excitatory (TP, PTP) responses, approaching normal levels.
These findings, in conjunction with the previous research on the protective role of hydrocortisone in depressive reactions, suggest that hydrocortisone effectively mitigates excitotoxicity and provides significant neuroprotection in the context of PD.
抗伤害感受中枢参与大脑内的神经退行性变,尤其是在伴有慢性疼痛的帕金森病(PD)中,目前尚未完全明确。
对15只白化大鼠在三种实验条件下进行电生理记录:完整状态、鱼藤酮诱导的PD模型以及用氢化可的松治疗的PD模型。记录中脑导水管周围灰质(PAG)中241个单个神经元对中缝大核(RMG)刺激的细胞外锋电位活动。
PD模型在记录的神经元中表现出显著的兴奋性毒性,表明存在大量神经退行性变,这似乎先于刺激后的抑制性(强直后抑制[TD]、强直后增强[PTD])和兴奋性(强直增强[TP]、强直后增强[PTP])效应。对刺激前后激活频率的数学分析显示:在氢化可的松保护的PD模型中,与未保护的PD模型相比,RMG高频刺激期间PAG神经元的刺激前激活频率降低,使其值更接近正常水平。治疗组PAG神经元的刺激后激活频率在抑制性(TD、PTD)和兴奋性(TP、PTP)反应中也降低,接近正常水平。
这些发现,结合先前关于氢化可的松在抑郁反应中的保护作用的研究,表明氢化可的松可有效减轻兴奋性毒性,并在PD背景下提供显著的神经保护作用。