帕金森病模型中大鼠丘脑腹侧后外侧核(vpl)神经元对体感器核心刺激反应的脉冲活动动力学

G. Musheghyan, G. Arajyan, М. V. Poghosyan, J. Sarkissian
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引用次数: 0

摘要

随着预期寿命的延长,神经退行性疾病将会增加。大多数神经退行性疾病(ND)患者主诉疼痛,其起源在很大程度上仍然未知,需要进一步研究。疼痛和PD的话题难以解决的原因之一是,有时很难辨别特定的疼痛是否是由PD引起的。慢性疼痛在普通人群中是一种常见的症状,PD患者也不能对常见的问题免疫。然而,PD的某些方面可能会加剧常见问题带来的疼痛。此外,PD患者可能会有一些特殊类型的疼痛。作为最重要的非运动症状,帕金森氏病的疼痛发作频繁且更强烈,这违反了疼痛的情绪测量和对其强度的主观感知。此外,PD中还描述了各种类型的疼痛,主要是神经性或伤害性疼痛。在治疗建议中,疼痛症状的出现通常不被考虑在内,使其管理只能由医生自行决定。关注此类疾病疼痛频率的研究表明,帕金森病(PD)在选定人群中的疼痛患病率很高,从40%到86%不等。不同的研究评估疼痛的方法不同,因此疼痛的类型很少被报道。然而,普遍的非神经性疼痛来源出现了PD。对8只白化系大鼠(230±30g)进行了电生理实验,其中完整体(5只)和鱼藤酮帕金森病模型(3只)。对丘脑腹后外侧核(nVPL) 229个单个神经元在高频刺激大脑第二体感皮层时的脉冲活动进行了细胞外记录。在上述条件下,破伤风抑制反应和兴奋反应发生变化,并伴有破伤风后抑制反应和增强反应,根据以盘状图呈现的脉冲平均频率图,分析了抑制作用和兴奋作用的相对频率强度。在两个序列的PD模型上,与正常相比,抑制刺激后反应的神经元数量减少。在抑制序列和兴奋序列之前,nVPL神经元冲动活动的前刺激频率显著增加。PD模型上伴随抑制性和兴奋性序列的脉冲活动后刺激频率也明显增加。病理上刺激前和刺激后活动频率的显著变化是兴奋性毒性发展的结果,这充满了细胞凋亡和死亡。综上所述,在PD模型中,nVPL神经元表现出兴奋性毒性,导致丘脑这些重要的抗感觉结构的神经退行性失败,并产生抵抗性慢性疼痛。标记表明需要保护性保存抑制作用,减少过度兴奋。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
DYNAMICS OF THE IMPULSE ACTIVITY OF NEURONS IN THE VENTRAL POSTEROLATERAL NUCLEUS (VPL) OF THE RAT’S THALAMUS IN RESPONSE TO SOMATOSENSOR CORE STIMULATION IN A PARKINSON’S DISEASE MODEL
Neurodegenerative diseases are going to increase as the life expectancy is getting longer. Most patients with neurodegenerative diseases (ND) complain of pain, the origin of which remains largely unknown and requires further research. One of the reasons why the topic of pain and PD is difficult to address is that it is sometimes tough to discern whether a particular pain is due to PD or not. Chronic pain is such a common symptom among the general population, and people with PD are not immune to common problems as well. However, there are aspects of PD that may exacerbate the pain experienced from a common problem. In addition, there are particular types of pain that may be unique to people with PD. There is a frequent and more intense onset of pain in Parkinson’s disease, as the most important non-motor symptom, with a violation of both the emotional measurement of pain and the subjective perception of its intensity. In addition, various types of pain have been described in PD, mainly neuropathic or nociceptive. The presence of pain symptoms is often not taken into account in the recommendations for treatment, leaving their management at the discretion of only doctors. Studies focusing on pain frequency in such disorders suggest a high prevalence of pain in selected populations from 40% to 86% in Parkinson’s disease (PD). The methods of pain assessment vary between studies so the type of pain has been rarely reported. However, a prevalent nonneuropathic origin of pain emerged for PD. The electrophysiological investigations on 8 rats Albino lines (230±30g.) has been conducted: intacts (5 animals) and on the rotenone model of Parkinson’s disease (PD) (3 animals) has been conducted. The extracellular recording of impulse activity 229 single neurons of ventral-posterolateral nucleus (nVPL) of thalamus on high frequency stimulation of second somatosensory cortex of the brain has been produced. Analyses of relative degree frequency intensity of depressor and excitatory effects, on the bases of diagrams of average frequency of impulses, presented as disk graphs in mentioned conditions following changes of tetanic depressor and excitatory reactions, accompanied by posttetanic depressor and potentiation has been revealed. On the model of PD in both sequences, in comparison with norm, reduction in the number of neurons, responded by inhibitory poststimulus reactions has been revealed. The prestimulus frequency of nVPL neurons impulse activity, preceding to both inhibitory and excitatory sequences, in comparison with, dramatically increased turned out to be. The poststimulus frequency of impulse activity on the model of PD, accompanied by inhibitory and excitatory sequences also significantly increased turned out to be. A significant shift of frequency of pre- and poststimulus activity in pathology is a consequence of the development of excitotoxicity, that is fraught with apoptosis and dead. In conclusion, on the model of PD the excitotoxicity revealed in neurons of nVPL, leading to neurodegenerative defeat of these important antinociceptive structures of thalamus, with origin of resistant chronic pain. Marked indicates the need of protective conservation of inhibitory effects and reduced of excessive excitatory.
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