Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California, USA.
Veterans Administration Greater Los Angeles HealthCare System, Sepulveda, Los Angeles, Los Angeles, California, USA.
Mov Disord. 2017 Dec;32(12):1687-1693. doi: 10.1002/mds.27133. Epub 2017 Aug 26.
Abnormal striatal dopamine transmission has been hypothesized to cause restless legs syndrome. Dopaminergic drugs are commonly used to treat restless legs syndrome. However, they cause adverse effects with long-term use. An animal model would allow the systematic testing of potential therapeutic drugs. A high prevalence of restless legs syndrome has been reported in iron-deficient anemic patients. We hypothesized that the iron-deficient animal would exhibit signs similar to those in restless legs syndrome patients.
After baseline polysomnographic recordings, iron-deficient rats received pramipexole injection. Then, iron-deficient rats were fed a standard rodent diet, and polysomnographic recording were performed for 2 days each week for 4 weeks.
Iron-deficient rats have low hematocrit levels and show signs of restless legs syndrome: sleep fragmentation and periodic leg movements in wake and in slow-wave sleep. Iron-deficient rats had a positive response to pramipexole treatment. After the iron-deficient rats were fed the standard rodent diet, hematocrit returned to normal levels, and sleep quality improved, with increased average duration of wake and slow-wave sleep episodes. Periodic leg movements decreased during both waking and sleep. Hematocrit levels positively correlated with the average duration of episodes in wake and in slow-wave sleep and negatively correlated with periodic leg movements in wake and in sleep. Western blot analysis showed that striatal dopamine transporter levels were higher in iron-deficient rats.
The iron-deficient rat is a useful animal model of iron-deficient anemic restless legs syndrome. © 2017 International Parkinson and Movement Disorder Society.
异常纹状体多巴胺传递被认为会导致不宁腿综合征。多巴胺能药物常用于治疗不宁腿综合征。然而，它们会在长期使用后引起不良反应。动物模型将允许对潜在治疗药物进行系统测试。缺铁性贫血患者中报告了不宁腿综合征的高患病率。我们假设缺铁动物会表现出与不宁腿综合征患者相似的症状。
在基线多导睡眠记录后，缺铁大鼠接受普拉克索注射。然后，缺铁大鼠喂食标准啮齿动物饮食，每周进行两次多导睡眠记录，持续 4 周。
缺铁大鼠的血细胞比容水平较低，并表现出不宁腿综合征的迹象：睡眠碎片化和清醒及慢波睡眠中的周期性腿部运动。缺铁大鼠对普拉克索治疗有积极反应。缺铁大鼠喂食标准啮齿动物饮食后，血细胞比容恢复正常，睡眠质量改善，清醒和慢波睡眠的平均持续时间增加。在清醒和睡眠期间周期性腿部运动减少。血细胞比容水平与清醒和慢波睡眠中的平均持续时间呈正相关，与清醒和睡眠中的周期性腿部运动呈负相关。Western blot 分析显示，缺铁大鼠纹状体多巴胺转运体水平较高。
缺铁大鼠是一种有用的缺铁性贫血不宁腿综合征动物模型。© 2017 年国际帕金森病和运动障碍学会。
