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The preventive effects of ascorbic acid supplementation on locomotor and acetylcholinesterase activity in an animal model of schizophrenia induced by ketamine

机译:抗坏血酸补充对氯胺酮诱导性精神分裂症动物模型运动与乙酰胆碱酯酶活性的预防作用

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Studies have shown that schizophrenic patients seem to have nutritional deficiencies. Ascorbic acid (AA) has an important antioxidant effect and neuromodulatory properties. The aim of this study was to evaluate the effects of AA on locomotor activity and the acetylcholinesterase activity (AChE) in an animal model of schizophrenia (SZ). Rats were supplemented with AA (0.1, 1, or 10 mg/kg), or water for 14 days (gavage). Between the 9th and 15th days, the animals received Ketamine (Ket) (25 mg/kg) or saline (i.p). After the last administration (30 min) rats were subjected to the behavioral test. Brain structures were dissected for biochemical analysis. There was a significant increase in the locomotor activity in Ket treated. AA prevented the hyperlocomotion induced by ket. Ket also showed an increase of AChE activity within the prefrontal cortex and striatum prevented by AA. Our data indicates an effect for AA in preventing alterations induced by Ket in an animal model of SZ, suggesting that it may be an adjuvant approach for the development of new therapeutic strategies within this psychiatric disorder.
机译:研究表明,精神分裂症患者似乎具有营养缺陷。抗坏血酸(AA)具有重要的抗氧化效果和神经调节性能。本研究的目的是评估AA对精神分裂症(SZ)动物模型中运动活性和乙酰胆碱酯酶活性(ACHE)的影响。将大鼠补充有AA(0.1,1或10mg / kg)或水14天(GavaGe)。在第9天之间,动物接受氯胺酮(KET)(25mg / kg)或盐水(I.p)。最后一次施用(30分钟)大鼠进行行为试验后。解剖脑结构进行生化分析。 KET治疗的运动活性有显着增加。 AA阻止了KET引起的高胎面。 KET还显示出在前额叶皮质和纹状体内的疼痛活性的增加。我们的数据表明AA在防止SZ的动物模型中防止KET诱导的改变的效果,表明它可能是在这种精神疾病中开发新的治疗策略的辅助方法。

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