Neuronal activity is the main contributor to the high-energy demand of the human brain. ATP is needed for the maintenance of ionic gradients, neurotransmitter transport, and release, as well as the signaling pathways that follow activation of post-synaptic receptors. The inability to maintain a high supply of ATP through tight regulatory mechanisms can, therefore, have severe consequences for brain function. In this issue of EMBO Reports, Cui et al [1] show that pharmacological inhibition or genetic inactivation of CD39, an ectonucleotide tri(di)phosphohydrolase responsible for converting ATP into AMP, has antidepressant-like effects by maintaining high extracellular ATP levels in the presence of stress.

中文翻译：

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抑郁症：一种新的酶 AT 发挥作用。


神经元活动是人脑高能量需求的主要贡献者。 ATP 是维持离子梯度、神经递质运输和释放以及突触后受体激活后的信号传导途径所必需的。因此，无法通过严格的调节机制维持 ATP 的高供应可能会对大脑功能产生严重后果。在本期 EMBO 报告中，Cui 等人 [1] 表明，CD39（一种负责将 ATP 转化为 AMP 的核苷酸三（二）磷酸水解酶）的药理学抑制或基因灭活，通过在细胞内维持高细胞外 ATP 水平而具有抗抑郁样作用。压力的存在。