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首页> 外文期刊>Cell cycle >Antidepressants and Cdk inhibitors: releasing the brake on neurogenesis?
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Antidepressants and Cdk inhibitors: releasing the brake on neurogenesis?

机译：抗抑郁药和Cdk抑制剂：释放神经发生的刹车？

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It is now clear that neurogenesis occurs in the brain of adult mammals. Many studies have attempted to establish relationships among neurogenesis, depression and the mechanism of action of antidepressant drugs. Therapeutic effects of antidepressants appear to be linked to increased neurogenesis in the hippocampus. Cdk inhibitors are expressed in multiple brain regions, presumably maintaining quiescence in differentiated neurons. Recently, the abundant expression of p21(Cip1) was found in neuroblasts and in newly developing neurons in the subgranular zone of the hippocampus, a region where adult neurogenesis occurs. Chronic treatment with the tricyclic antidepressant imipramine markedly decreased p21(Cip1) mRNA and protein levels and stimulated neurogenesis in this region. These results suggest that p21(Cip1) restrains neurogenesis in the hippocampus, and antidepressant-induced stimulation of neurogenesis might be a consequence of decreased p21(Cip1) expression, with the subsequent release of neuronal progenitor cells from the blockade of proliferation. These findings suggest the potential for new therapeutic strategies for the treatment of depression that target cell cycle proteins. However, there is a possibility that long-term stimulation of neurogenesis might exhaust the proliferation potentials of neuronal progenitors.
机译：现在很清楚，神经发生发生在成年哺乳动物的大脑中。许多研究试图建立神经发生，抑郁与抗抑郁药作用机制之间的关系。抗抑郁药的治疗作用似乎与海马神经发生的增加有关。 Cdk抑制剂在多个大脑区域表达，大概在分化的神经元中保持静止。最近，p21（Cip1）的大量表达被发现在成神经细胞和海马的亚颗粒区的新生神经元中，该区域发生成人神经发生。长期用三环抗抑郁剂丙咪嗪治疗可明显降低p21（Cip1）mRNA和蛋白质水平，并刺激该区域的神经发生。这些结果表明，p21（Cip1）抑制海马中的神经发生，而抗抑郁药诱导的神经发生刺激可能是p21（Cip1）表达降低的结果，随后神经元祖细胞从增殖阻滞中释放出来。这些发现提示了针对靶向细胞周期蛋白的抑郁症的新治疗策略的潜力。但是，长期刺激神经发生可能会耗尽神经元祖细胞的增殖潜能。

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