Hippocampal neurogenesis: a biomarker for depression or antidepressant effects? Methodological considerations and perspectives for future research

Hippocampal neurogenesis: a biomarker for depression or antidepressant effects? Methodological considerations and perspectives for future research
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DOI:
10.1007/s00441-013-1612-z
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发表时间:
2013-04
影响因子:
3.6
通讯作者:
A. Tanti;C. Belzung
A. Tanti;C. Belzung
中科院分区:
生物学3区
文献类型:
--
作者:
A. Tanti;C. Belzung

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Whereas animal models of depression are associated with decreased adult hippocampal neurogenesis, antidepressant treatments, including pharmacotherapy but also electroconvulsive therapy, have the opposite action, as they stimulate cell proliferation and the survival and maturation of newborn dentate gyrus neurons. Although the lack of these new cells is not causally involved in depression, as their absence does not trigger a depressive-episodeper se, their loss has been shown to be causally involved in the ability of chronic monoaminergic antidepressants to achieve remission. However, the process by which the stimulation of hippocampal neurogenesis can elicit recovery after a depressive-like episode is poorly understood. The accepted view is that hippocampal newborn neurons integrate into the hippocampal network and thus participate in hippocampal cognitive functions crucial for remission. The hippocampus is associated with a wide range of such functions, including spatial navigation, pattern separation, encoding of new contextual information, emotional behavior and control over the hypothalamic-pituitary-adrenal axis. The present review aims at discussing each of these functions and tries to identify the process by which newborn cells participate in remission after successful therapy. Finally, future directions are proposed for a better understanding of these mechanisms.