Malberg J E, Eisch A J, Nestler E J, Duman R S
Laboratory of Molecular Psychiatry, Departments of Psychiatry and Pharmacology, Yale University School of Medicine, Connecticut Mental Health Center, New Haven, Connecticut 06508, USA.
J Neurosci. 2000 Dec 15;20(24):9104-10. doi: 10.1523/JNEUROSCI.20-24-09104.2000.
Recent studies suggest that stress-induced atrophy and loss of hippocampal neurons may contribute to the pathophysiology of depression. The aim of this study was to investigate the effect of antidepressants on hippocampal neurogenesis in the adult rat, using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells. Our studies demonstrate that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of several different classes of antidepressant, but not non-antidepressant, agents was found to increase BrdU-labeled cell number, indicating that this is a common and selective action of antidepressants. In addition, upregulation of the number of BrdU-labeled cells is observed after chronic, but not acute, treatment, consistent with the time course for the therapeutic action of antidepressants. Additional studies demonstrated that antidepressant treatment increases the proliferation of hippocampal cells and that these new cells mature and become neurons, as determined by triple labeling for BrdU and neuronal- or glial-specific markers. These findings raise the possibility that increased cell proliferation and increased neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of hippocampal neurons and may contribute to the therapeutic actions of antidepressant treatment.
最近的研究表明,应激诱导的海马神经元萎缩和丧失可能在抑郁症的病理生理学中起作用。本研究的目的是使用胸腺嘧啶类似物溴脱氧尿苷(BrdU)作为分裂细胞的标志物,研究抗抑郁药对成年大鼠海马神经发生的影响。我们的研究表明,慢性抗抑郁药治疗可显著增加海马齿状回和海马体中BrdU标记细胞的数量。发现给予几种不同类别的抗抑郁药而非非抗抑郁药可增加BrdU标记细胞的数量,表明这是抗抑郁药的一种常见且选择性的作用。此外,在慢性而非急性治疗后观察到BrdU标记细胞数量上调,这与抗抑郁药的治疗作用时间进程一致。进一步的研究表明,抗抑郁药治疗可增加海马细胞的增殖,并且这些新细胞成熟并成为神经元,这是通过对BrdU以及神经元或胶质细胞特异性标志物进行三重标记确定的。这些发现提出了一种可能性,即细胞增殖增加和神经元数量增加可能是抗抑郁药治疗克服应激诱导的海马神经元萎缩和丧失的一种机制,并且可能有助于抗抑郁药治疗的疗效。