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Is the 5-HT2C receptor a therapeutic target in cerebral ischaemia?

机译:5-HT2C受体是脑缺血的治疗靶点吗?

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This study examines the effect of a 5-HT2C agonist (RO 60-0175, (s)-2-(chloro-5-fluoro-indol-1-yl)-1-methylethylamine) and a 5-HT2C antagonist (RO 43-0440, benzofuran-2-carboxamidine) for neuroprotective activity in a rat model of global cerebral ischaemia. A mini-osmotic pump implanted subcutaneously delivered 0.25 mg/kg/hr. Seven days after ischaemia the rats were sacrificed and the damage in the CA1 pyramidal cell layer in hippocampus was estimated and the treated groups were compared with vehicle groups. Pretreatment with the 5-HT2C agonist RO 60-0175 significantly increased the damage, whereas the 5-HT2C antagonist RO 43-0440 had no effect on the cell damage. Measurement of the core temperature in a RO 60-0175-treated group of rats revealed no effect compared to a vehicle-treated group. Thus the aggravation of damage in the RO 60-0175-treated group cannot be explained by temperature effect. Our data do not indicate the 5-HT2C receptor as a therapeutic target in cerebral ischaemia.
机译:这项研究检查了5-HT2C激动剂(RO 60-0175,(s)-2-(氯-5-氟-吲哚-1-基)-1-甲基乙胺)和5-HT2C拮抗剂(RO 43 -0440,苯并呋喃-2-羧am)对全脑缺血的大鼠具有神经保护作用。皮下植入的微型渗透泵的流量为0.25 mg / kg / hr。缺血7天后处死大鼠,并估计海马CA1锥体细胞层的损伤,并将治疗组与溶媒组进行比较。用5-HT2C激动剂RO 60-0175进行的预处理显着增加了损伤,而5-HT2C拮抗剂RO 43-0440对细胞损伤没有影响。 RO 60-0175治疗组大鼠的核心温度测量结果显示,与溶媒治疗组相比,无任何影响。因此,RO 60-0175处理组的损伤加剧无法通过温度效应来解释。我们的数据没有表明5-HT2C受体是脑缺血的治疗靶点。

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