Environmental enrichment inhibits spontaneous apoptosis, prevents seizuresand is neuroprotective

Citation
D. Young et al., Environmental enrichment inhibits spontaneous apoptosis, prevents seizuresand is neuroprotective, NAT MED, 5(4), 1999, pp. 448-453
Citations number
45
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
NATURE MEDICINE
ISSN journal
10788956 → ACNP
Volume
5
Issue
4
Year of publication
1999
Pages
448 - 453
Database
ISI
SICI code
1078-8956(199904)5:4<448:EEISAP>2.0.ZU;2-J
Abstract
The mammalian brain has a high degree of plasticity, with dentate granule c ell neurogenesis(1) and glial(2,3) proliferation stimulated by an enriched environment combining both complex inanimate and social stimulation. Moreov er, rodents exposed to an enriched environment both before and after a cere bral insult show improved cognitive performance(1,4). One of the most robus t associations of environmental enrichment is improved learning and memory in the Morris water maze, a spatial task that mainly involves the hippocamp us(5). Furthermore, clinical evidence showing an association between higher educational attainment and reduced risk of Alzheimer(6) and Parkinson-rela ted dementia(7) indicates that a stimulating environment has positive effec ts 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-i nduced seizures and excitotoxic injury. The enriched environment induces ex pression of glial-derived neurotrophic factor and brain-derived neurotrophi c factor and increases phosphorylation of the transcription factor cyclic-A MP 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 growt h factor expression.