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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Methylphenidate alters NCS-1 expression in rat brain.
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Methylphenidate alters NCS-1 expression in rat brain.

机译：哌醋甲酯改变大鼠脑中NCS-1的表达。

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Methylphenidate has been used as an effective treatment for attention deficit hyperactivity disorder (ADHD). Methylphenidate (MPH) blocks dopamine and norepinephrine transporters causing an increase in extracellular levels. The use of psychomotor stimulants continues to rise due to both the treatment of ADHD and illicit abuse. Methylphenidate sensitization mechanism has still poor knowledge. Neuronal calcium sensor 1 was identified as a dopaminergic receptor interacting protein. When expressed in mammalian cells, neuronal calcium sensor 1 attenuates dopamine-induced D2 receptor internalization by a mechanism that involves a reduction in D2 receptor phosphorylation. Neuronal calcium sensor 1 appears to play a pivotal role in regulating D2 receptor function, it will be important to determine if there are alterations in neuronal calcium sensor 1 in neuropathologies associated with deregulation in dopaminergic signaling. Then, we investigated if methylphenidate could alter neuronal calcium sensor 1 expression in five brain regions (striatum, hippocampus, prefrontal cortex, cortex and cerebellum) in young and adult rats. These regions were chosen because some are located in brain circuits related with attention deficit hyperactivity disorder. Our results showed changes in neuronal calcium sensor 1 expression in hippocampus, prefrontal cortex and cerebellum mainly in adult rats. The demonstration that methylphenidate induces changes in neuronal calcium sensor 1 levels in rat brain may help to understand sensitization mechanisms as well as methylphenidate therapeutic effects to improve attention deficit hyperactivity disorder symptoms.
机译：哌醋甲酯已被用作注意力缺陷多动障碍（ADHD）的有效治疗方法。哌醋甲酯（MPH）阻止多巴胺和去甲肾上腺素转运蛋白，导致细胞外水平增加。由于多动症的治疗和非法滥用，精神运动兴奋剂的使用继续增加。哌醋甲酯的敏化机理仍知之甚少。神经元钙传感器1被确定为多巴胺能受体相互作用蛋白。当在哺乳动物细胞中表达时，神经元钙传感器1通过减少D2受体磷酸化的机制减弱多巴胺诱导的D2受体内在化。神经元钙传感器1似乎在调节D2受体功能中起着关键作用，确定与多巴胺能信号传导失调相关的神经病理学中神经元钙传感器1的改变将很重要。然后，我们调查了哌醋甲酯是否可以改变年轻和成年大鼠五个大脑区域（纹状体，海马，前额叶皮层，皮层和小脑）中神经元钙传感器1的表达。选择这些区域是因为某些区域位于与注意力缺陷多动障碍相关的脑回路中。我们的研究结果显示，成年大鼠海马，前额叶皮层和小脑中神经元钙传感器1表达的变化。哌醋甲酯可诱导大鼠大脑神经元钙传感器1水平发生变化的证据可能有助于理解致敏机制以及哌醋甲酯对改善注意力缺陷多动障碍症状的治疗作用。

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