Environmental enrichment inhibits spontaneous apoptosis, prevents seizures and is neuroprotective

被引:615
作者
Young, D
Lawlor, PA
Leone, P
Dragunow, M
During, MJ [1 ]
机构
[1] Univ Auckland, Sch Med, Dept Mol Med, Auckland 1, New Zealand
[2] Thomas Jefferson Univ, Jefferson Med Coll, Dept Neurosurg, Philadelphia, PA 19107 USA
关键词
D O I
10.1038/7449
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The mammalian brain has a high degree of plasticity, with dentate granule cell neurogenesis(1) and glial(2,3) proliferation stimulated by an enriched environment combining both complex inanimate and social stimulation. Moreover, rodents exposed to an enriched environment both before and after a cerebral insult show improved cognitive performance(1,4). One of the most robust associations of environmental enrichment is improved learning and memory in the Morris water maze, a spatial task that mainly involves the hippocampus(5). Furthermore, clinical evidence showing an association between higher educational attainment and reduced risk of Alzheimer(6) and Parkinson-related dementia(7) indicates that a stimulating environment has positive effects on cerebral health that may provide some resilience to cerebral insults. Here we show that in addition to its effects on neurogenesis, an enriched environment reduces spontaneous apoptotic cell death in the rat hippocampus by 45%. Moreover, these environmental conditions protect against kainate-induced seizures and excitotoxic injury. The enriched environment induces expression of glial-derived neurotrophic factor and brain-derived neurotrophic factor and increases phosphorylation of the transcription factor cyclic-AMP response element binding protein, indicating that the; influence of the environment on spontaneous apoptosis and cerebral resistance to insults may be mediated through transcription factor activation and induction of growth factor expression.
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收藏
页码:448 / 453
页数:6
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