Journal
JOURNAL OF NEUROSCIENCE
Volume 25, Issue 41, Pages 9328-9338Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2281-05.2005
Keywords
memory; long-term potentiation; aging; hippocampus; stress; dendritic atrophy
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Funding
- NIA NIH HHS [T32 AG000096, T32 AG00096] Funding Source: Medline
- NINDS NIH HHS [R01 NS039307-02, R01 NS028912-09, R01 NS039307-04, NS39307, R01 NS028912, R01 NS028912-08, NS28912, R01 NS039307, R01 NS028912-10, P01 NS045260, R01 NS039307-03, NS045260] Funding Source: Medline
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Progressive cognitive deficits that emerge with aging are a result of complex interactions of genetic and environmental factors. Whereas much has been learned about the genetic underpinnings of these disorders, the nature of acquired contributing factors, and the mechanisms by which they promote progressive learning and memory dysfunction, remain largely unknown. Here, we demonstrate that a period of early-life psychological stress causes late-onset, selective deterioration of both complex behavior and synaptic plasticity: two forms of memory involving the hippocampus, were severely but selectively impaired in middle-aged, but not young adult, rats exposed to fragmented maternal care during the early postnatal period. At the cellular level, disturbances to hippocampal long-term potentiation paralleled the behavioral changes and were accompanied by dendritic atrophy and mossy fiber expansion. These findings constitute the first evidence that a short period of stress early in life can lead to delayed, progressive impairments of synaptic and behavioral measures of hippocampal function, with potential implications to the basis of age-related cognitive disorders in humans.
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