School of Biology, Damghan University, Damghan, Iran.
Eur J Pharmacol. 2012 Nov 15;695(1-3):40-7. doi: 10.1016/j.ejphar.2012.08.014. Epub 2012 Sep 5.
Essential tremor (ET) is one of the most common and most disabling movement disorders among adults. The drug treatment of essential tremor remains unsatisfactory. Additional therapies are required for patients with inadequate response or intolerable side effects. Thus, we aimed to investigate the therapeutic effects of riluzole on harmaline-induced tremor and ataxia in rat, and determining whether riluzole exerts its effect through modulation of glutamate levels in cerebellum. The study included 5 groups of Wistar rats weighing 80-100g, injected with harmaline (50mg/kg i.p.) for inducing experimental tremors and ataxia. The rats in group 1 served as control (saline induced) and group 2 received harmaline alone, whereas the animals in groups 3, 4 and 5, were also given riluzole intraperitoneally at doses of 2, 4 and 8 mg/kg 10 min after harmaline administration, respectively. The intensity and duration of tremor were recorded. Rotarod test, distance traveled and number of crossings were used to evaluate motor performance. Results of this study demonstrated that riluzole dose dependently attenuated duration and intensity of harmaline-induced tremors. Also, riluzole significantly improves time to fall, distance traveled and number of crossings in combined riluzole and harmaline treated rats. Histological analysis indicated that harmaline could cause vermis Purkinje cell (PC) loss and riluzole prevented this toxic effect. Harmaline also could increase glutamate levels in vermis and treatment with riluzole restored glutamate levels. In conclusion, riluzole has relatively protective effects on harmaline-induced tremor, probably related to its inhibitory effect on glutamatergic neurotransmission.
特发性震颤(ET)是成年人中最常见和最致残的运动障碍之一。特发性震颤的药物治疗仍然不尽如人意。对于反应不足或无法耐受副作用的患者,需要额外的治疗方法。因此,我们旨在研究利鲁唑对哈尔明诱导的震颤和大鼠共济失调的治疗作用,并确定利鲁唑是否通过调节小脑谷氨酸水平发挥作用。
这项研究包括 5 组体重为 80-100g 的 Wistar 大鼠,腹腔注射哈尔明(50mg/kg)诱导实验性震颤和共济失调。第 1 组大鼠作为对照(生理盐水诱导),第 2 组单独给予哈尔明,而第 3、4 和 5 组大鼠在给予哈尔明后 10 分钟内也分别给予利鲁唑 2、4 和 8mg/kg 腹腔内注射。记录震颤的强度和持续时间。转棒试验、行驶距离和穿越次数用于评估运动表现。
研究结果表明,利鲁唑剂量依赖性地减轻了哈尔明诱导的震颤的持续时间和强度。此外,利鲁唑显著提高了联合利鲁唑和哈尔明治疗大鼠的跌倒时间、行驶距离和穿越次数。组织学分析表明,哈尔明可导致小脑绒球 Purkinje 细胞(PC)丢失,而利鲁唑可预防这种毒性作用。哈尔明还可增加绒球谷氨酸水平,而利鲁唑治疗可恢复谷氨酸水平。
总之,利鲁唑对哈尔明诱导的震颤具有相对保护作用,可能与其抑制谷氨酸能神经传递有关。