PDF(Pubmed)
Abstract：
Patients with vascular dementia experience more pain than healthy elders, potentially due to the presence of central neuropathic pain. However, the mechanisms underlying neuropathic pain in vascular dementia remain poorly understood, and there is currently a lack of effective treatment available. In this study, a rat model of vascular dementia was induced by permanently occluding the common carotid arteries bilaterally (2-VO). The cognitive impairments in the 2-VO rats were evaluated using the Morris Water Maze test, while HE and LBF staining were employed to assess brain tissue lesions in the hippocampal, cerebral cortex, and white matter regions known to be associated with severe memory and learning deficits. Furthermore, pain-related behavioral tests, including mechanical and thermal stimuli assessments, were conducted, and in vivo electrophysiological recordings of primary sensory neurons were performed. Compared to sham-operated and pre-operative rats, rats with vascular dementia exhibited mechanical allodynia and thermal hyperalgesia 30 days after surgery. Furthermore, in vivo electrophysiology revealed a significant increase in the occurrence of spontaneous activity of Aβ- and C-fiber sensory neurons in the rat model of vascular dementia. These results indicate that neuropathic pain behaviors developed in the rat model of vascular dementia, and abnormal spontaneous discharges of primary sensory neurons may play a crucial role in the development of pain after vascular dementia.
摘要：
血管性痴呆患者比健康的老年人更痛苦,可能是由于中枢神经疼痛的存在。然而,血管性痴呆神经性疼痛的潜在机制仍然知之甚少，目前缺乏有效的治疗方法。在这项研究中,通过永久闭塞双侧颈总动脉（2-VO）诱导血管性痴呆大鼠模型。使用Morris水迷宫测试评估2-VO大鼠的认知障碍，而HE和LBF染色用于评估海马的脑组织病变，大脑皮层,和已知与严重记忆和学习缺陷有关的白质区域。此外，疼痛相关行为测试,包括机械和热刺激评估，进行了，并进行了初级感觉神经元的体内电生理记录。与假手术和手术前大鼠相比，血管性痴呆大鼠术后30天出现机械性异常疼痛和热痛觉过敏。此外，体内电生理显示，在血管性痴呆大鼠模型中，Aβ和C纤维感觉神经元的自发活动显着增加。这些结果表明，在血管性痴呆的大鼠模型中发生了神经性疼痛行为，初级感觉神经元的异常自发放电可能在血管性痴呆后疼痛的发展中起关键作用。
