Fibromyalgia (FM) is a complex syndrome, with an indefinite aetiology and intricate pathophysiology that affects 2 – 3% of the world population. From the beginning of the 2000s, experimental animal models have been developed to mimic clinical FM and help obtain a better understanding of the relevant neurobiology. These animal models have enabled a broad study of FM symptoms and mechanisms, as well as new treatment strategies. Current experimental FM models include the reserpine-induced systemic depletion of biogenic amines, muscle application of acid saline, and stress-based (cold, sound, or swim) approaches, among other emerging models. FM models should: (i) mimic the cardinal symptoms and complaints reported by FM patients (e.g., spontaneous nociception, muscle pain, hypersensitivity); (ii) mimic primary comorbidities that can aggravate quality of life and lead to worse outcomes (e.g., fatigue, sleep disturbance, depression, anxiety); (iii) mimic the prevalent pathological mechanisms (e.g., peripheral and central sensitization, inflammation/neuroinflammation, change in the levels of the excitatory and inhibitory neurotransmitters); and (iv) demonstrate a pharmacological profile similar to the clinical treatment of FM. However, it is difficult for any one of these models to include the entire spectrum of clinical FM features once even FM patients are highly heterogeneous. In the past six years (2015 – 2020), a wide range of experimental FM studies has amounted to the literature reinforcing the need for an updated review. Here we have described, in detail, several approaches used to experimentally study FM, with a focus on recent studies in the field and in previously less discussed mechanisms. We highlight each model’s challenges, limitations, and future directions, intending to help preclinical researchers establish the correct experimental FM model to use depending on their goals.

纤维肌痛 (FM) 是一种复杂的综合征，具有不确定的病因和复杂的病理生理学，影响世界 2-3% 的人口。从 2000 年代开始，已经开发出实验动物模型来模拟临床 FM 并帮助更好地了解相关的神经生物学。这些动物模型使对 FM 症状和机制以及新的治疗策略的广泛研究成为可能。目前的实验性 FM 模型包括利血平诱导的生物胺系统消耗、酸性盐水的肌肉应用和基于压力（冷、声音或游泳）的方法，以及其他新兴模型。FM 模型应该： (i) 模仿 FM 患者报告的主要症状和主诉（例如，自发性伤害感受、肌肉疼痛、超敏反应）；(ii) 模仿可加重生活质量并导致更坏结果的主要合并症（例如，疲劳、睡眠障碍、抑郁、焦虑）；(iii) 模拟流行的病理机制（例如，外周和中枢致敏、炎症/神经炎症、兴奋性和抑制性神经递质水平的变化）；(iv) 表现出与 FM 临床治疗相似的药理学特征。然而，一旦 FM 患者具有高度异质性，这些模型中的任何一个都很难包含整个临床 FM 特征谱。在过去六年（2015 年至 2020 年）中，大量的实验性 FM 研究已成为文献，强化了更新综述的必要性。在这里，我们详细描述了用于实验研究 FM 的几种方法，重点关注该领域的最新研究以及以前较少讨论的机制。我们强调每个模型的挑战、局限性和未来方向，旨在帮助临床前研究人员建立正确的实验 FM 模型，以根据他们的目标使用。