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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Possible mechanism of action in melatonin attenuation of haloperidol-induced orofacial dyskinesia.
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Possible mechanism of action in melatonin attenuation of haloperidol-induced orofacial dyskinesia.

机译：褪黑素减弱氟哌啶醇诱导的口面运动障碍的可能作用机制。

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摘要

Tardive dyskinesia (TD) is a late complication of prolonged neuroleptic treatment characterized by involuntary movements of the oral region. In spite of high incidence and much research, the pathophysiology of this devastating movement disorder remains elusive. Chronic treatment with neuroleptics leads to the development of abnormal oral movements in rats, referred to as vacuous chewing movements (VCMs). VCMs in rats are widely accepted as an animal model of TD. Rats chronically treated with haloperidol (1.5 mg/kg ip) significantly developed VCMs and tongue protrusions. Melatonin dose-dependently (1, 2, and 5 mg/kg) reversed the haloperidol-induced VCM and tongue protrusions frequencies. Biochemical analysis reveals that chronic haloperidol treatment significantly induced lipid peroxidation and decreased the forebrain glutathione (GSH) levels in the rats. Chronic haloperidol-treated rats also showed decreased levels of antioxidant defense enzymes, superoxide dismutase (SOD), and catalase. Coadministration of melatonin (1, 2, and 5 mg/kg) along with haloperidol significantly reduced the lipid peroxidation and restored the decreased GSH levels by chronic haloperidol treatment, and significantly reversed the haloperidol-induced decrease in forebrain SOD and catalase levels in rats. However, a lower dose of melatonin (1 mg/kg) failed to reverse chronic haloperidol-induced decreases in forebrain GSH, SOD, and catalase levels. In conclusion, melatonin could be screened as a potential drug candidate for the prevention or treatment of neuroleptic-induced orofacial dyskinesia.
机译：迟发性运动障碍（TD）是长期的抗精神病药物治疗的晚期并发症，其特征是口腔区域不自主运动。尽管发生率很高并且进行了大量研究，但是这种破坏性运动障碍的病理生理学仍然难以捉摸。用抗精神病药进行的长期治疗会导致大鼠出现异常的口腔运动，称为空腹咀嚼运动（VCM）。大鼠的VCM被广泛接受为TD的动物模型。氟哌啶醇（1.5 mg / kg ip）长期治疗的大鼠显着发展出VCM和舌头突出。褪黑激素剂量依赖性（1、2和5 mg / kg）逆转氟哌啶醇诱导的VCM和舌头突出的频率。生化分析表明，慢性氟哌啶醇治疗可显着诱导大鼠脂质过氧化并降低前脑谷胱甘肽（GSH）水平。慢性氟哌啶醇治疗的大鼠还显示出抗氧化防御酶，超氧化物歧化酶（SOD）和过氧化氢酶水平降低。褪黑素（1、2和5 mg / kg）与氟哌啶醇的共同给药可通过慢性氟哌啶醇治疗显着减少脂质过氧化并恢复降低的GSH水平，并显着逆转氟哌啶醇诱导的大鼠前脑SOD和过氧化氢酶水平的降低。但是，较低剂量的褪黑激素（1 mg / kg）未能逆转慢性氟哌啶醇引起的前脑GSH，SOD和过氧化氢酶水平的下降。总之，褪黑激素可以被筛选为预防或治疗精神安定药引起的口面运动障碍的潜在候选药物。

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