Neuronal plasticity and survival in mood disorders
Neuronal plasticity and survival in mood disorders
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DOI：
10.1016/s0006-3223(00)00935-5
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发表时间：
2000-10-15
影响因子：
10.6
通讯作者：
D'Sa, C
中科院分区：
文献类型：
--
作者：
Duman, RS;Malberg, J;D'Sa, C
基础和临床层面的研究表明，在应激反应以及抑郁症患者的大脑中会发生神经元萎缩和细胞死亡。尽管相关机制尚未完全阐明，但在描述中枢神经元萎缩和程序性细胞死亡的信号转导级联方面已经取得了进展，这些级联可能参与抗抑郁治疗的作用。这些通路包括环磷酸腺苷和神经营养因子信号转导级联。值得注意的是，这些相同的通路已被证实在神经可塑性的细胞模型中起着关键作用。这种可塑性和细胞存活通路的重叠，以及表明神经元活动可增强细胞存活的研究，都提示神经元萎缩和死亡可能是由神经可塑性的潜在机制被破坏所导致的。本文讨论了这些通路的作用以及神经元可塑性在应激相关情绪障碍中的失效，《生物精神病学》2000年；48卷：732 - 739页（C）2000生物精神病学学会。
Studies at the basic and clinical levels demonstrate that neuronal atrophy and cell death occur in response to stress and in the brains of depressed patients. Although the mechanisms have vet to be fully elucidated progress has been made in characterizing the signal transduction cascades that central neuronal atrophy and programmed cell death and that may be involved in the action of antidepressant treatment. These pathways include the cyclic adenosine monophosphate and neurotrophic factor signal transduction cascades. It is notable that these same pathways have been demonstrated to play a pivotal role in cellular models of neural plasticity. This over-lap of plasticity and cell survival pathways, together with studies demonstrating that neuronal activity enhances cell survival, suggests that neuronal atrophy and death could result from a disruption of the mechanisms underlying neural plasticity. The role of these pathways and failure of neuronal plasticity in stress-related mood disorders are discussed, Biol Psychiatry 2000;48:732-739 (C) 2000 Society of Biological Psychiatry.