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首页> 外文期刊>The European Journal of Neuroscience >Chronic activation of the D2 dopamine autoreceptor inhibits synaptogenesis in mesencephalic dopaminergic neurons in vitro.
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Chronic activation of the D2 dopamine autoreceptor inhibits synaptogenesis in mesencephalic dopaminergic neurons in vitro.

机译：D2多巴胺自身受体的慢性激活在体外抑制中脑多巴胺能神经元的突触形成。

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摘要

Chronic blockade or activation of dopamine receptors is critical for the pharmacological treatment of diseases like schizophrenia, Parkinson's or attention deficit and hyperactivity disorder. However, the long-term impact of such treatments on dopamine neurons is unclear. Chronic blockade of the dopamine D2 receptor in vivo triggers an increase in the axonal arborization of dopamine neurons [European Journal of Neuroscience, 2002, 16, 787-794]. However, the specific involvement of presynaptic (autoreceptors) vs. postsynaptic D2 receptors as well as the molecular mechanisms involved have not been determined. Here, we examined the role of D2 autoreceptors in regulating the ability of mouse dopamine neurons to establish axon terminals. Chronic activation of this receptor with quinpirole, a specific agonist, decreased the number of axon terminals established by isolated dopamine neurons. This effect was accompanied by a decrease in dopamine release and was mediated through inhibition of protein kinase A. The decrease in axon terminal number induced by D2 receptor activation was also occluded when the mammalian Target of Rapamycin pathway of mRNA translation was blocked. Our results suggest that chronic activation of the D2 autoreceptor inhibits synaptogenesis by mesencephalic dopamine neurons through translational regulation of the synthesis of proteins required for synapse formation. This study provides a better understanding of the impact of long-term pharmacological interventions acting through the D2 receptor.
机译：慢性阻断或激活多巴胺受体对于诸如精神分裂症，帕金森氏症或注意力缺陷和多动症等疾病的药物治疗至关重要。但是，这种治疗对多巴胺神经元的长期影响尚不清楚。体内多巴胺D2受体的慢性阻断触发了多巴胺神经元的轴突乔化[European Journal of Neuroscience，2002，16，787-794]。但是，尚未确定突触前（自体受体）与突触后D2受体的具体关系以及涉及的分子机制。在这里，我们检查了D2自身受体在调节小鼠多巴胺神经元建立轴突末端的能力中的作用。喹吡罗（一种特殊的激动剂）对该受体的慢性激活，减少了由孤立的多巴胺神经元建立的轴突末端的数量。这种作用伴随着多巴胺释放的减少，并通过抑制蛋白激酶A介导。当哺乳动物雷帕霉素靶标的mRNA翻译被阻断时，D2受体激活诱导的轴突末端数目的减少也被阻止。我们的研究结果表明，D2自身受体的慢性激活通过翻译调节突触形成所需蛋白的合成来抑制中脑多巴胺神经元的突触发生。这项研究更好地了解了通过D2受体起作用的长期药理学干预的影响。

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