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阿米替林和度洛西汀可减弱利血平诱导的纤维肌痛大鼠模型中背角浅层神经元的活动。

Amitriptyline and duloxetine attenuate activities of superficial dorsal horn neurons in a rat reserpine-induced fibromyalgia model.

机构信息

Department of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, 930-0194, Japan.

System Emotional Science, Faculty of Medicine, University of Toyama, Toyama, 930-0194, Japan; Department of Judo Therapy, Faculty of Medical Technology, Teikyo University, Utsunomiya, 320-8551, Japan.

出版信息

J Pharmacol Sci. 2024 Nov;156(3):180-187. doi: 10.1016/j.jphs.2024.08.006. Epub 2024 Aug 23.

Abstract

Fibromyalgia (FM) is an intractable disease with a chief complaint of chronic widespread pain. Amitriptyline (AMI) and duloxetine (DLX), which are antidepressant drugs, have been reported to ameliorate pain in patients with FM and pain-related behaviors in several rodent models of FM. However, the mechanisms of action of AMI and DLX are not yet fully understood. Here, we examined the effects of these drugs on the responsiveness of superficial dorsal horn (SDH) neurons in the spinal cord, using a rat FM model developed by injecting a biogenic amine depleter (reserpine). Extracellular recordings of SDH neurons in vivo demonstrated that bath application of AMI and DLX at concentrations of 0.1-1.0 mM on the dorsal surface of the spinal cord markedly suppressed spontaneous discharge and von Frey filament-evoked mechanical firing in SDH neurons. The suppression induced by the drugs was noted in a concentration-dependent manner and the suppressive effects resolved after washing the spinal cord surface. These results show that SDH neurons are the site of action for AMI and DLX in a rat reserpine-induced FM model. Spinal mechanisms may underlie the therapeutic effects of these drugs in patients with FM.

摘要

纤维肌痛(FM)是一种难以治愈的疾病,主要表现为慢性广泛性疼痛。三环类抗抑郁药阿米替林(AMI)和度洛西汀(DLX)已被报道可改善 FM 患者的疼痛和几种 FM 啮齿动物模型中的疼痛相关行为。然而,AMI 和 DLX 的作用机制尚不完全清楚。在这里,我们使用一种通过注射生物胺耗竭剂(利血平)开发的大鼠 FM 模型,检查了这些药物对脊髓背角浅层(SDH)神经元反应性的影响。在体 SDH 神经元的细胞外记录表明,在脊髓背表面以 0.1-1.0 mM 的浓度施加 AMI 和 DLX 可显著抑制 SDH 神经元的自发性放电和 von Frey 纤维诱发的机械放电。药物诱导的抑制作用呈浓度依赖性,洗涤脊髓表面后抑制作用得到解决。这些结果表明,SDH 神经元是 AMI 和 DLX 在大鼠利血平诱导的 FM 模型中的作用部位。脊髓机制可能是这些药物在 FM 患者中产生治疗效果的基础。

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