Stress and hippocampal plasticity

被引:1528
作者
McEwen, BS [1 ]
机构
[1] Rockefeller Univ, Harold & Margaret Milliken Hatch Lab Neuroendocri, New York, NY 10021 USA
关键词
glucocorticoids; NMDA receptors; dendrites; neurogenesis; memory; aging;
D O I
10.1146/annurev.neuro.22.1.105
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The hippocampus is a target of stress hormones, and it is an especially plastic and vulnerable region of the brain. It also responds to gonadal, thyroid, and adrenal hormones, which modulate changes in synapse formation and dendritic structure and regulate dentate gyrus volume during development and in adult life. Two forms of structural plasticity are affected by stress: Repeated stress causes atrophy of dendrites in the CA3 region, and both acute and chronic stress suppresses neurogenesis of dentate gyrus granule neurons. Besides glucocorticoids, excitatory amino acids and N-methyl-D-aspartate (NMDA) receptors are involved in these two forms of plasticity as well as in neuronal death that is caused in pyramidal neurons by seizures and by ischemia. The two forms of hippocampal structural plasticity are relevant to the human hippocampus, which undergoes a selective atrophy in a number of disorders, accompanied by deficits in declarative, episodic, spatial, and contextual memory performance. It is important, from a therapeutic standpoint, to distinguish between a permanent loss of cells and a reversible atrophy.
引用
收藏
页码:105 / 122
页数:18
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