![]() ![]() ![]() Repeated maternal separation, a potent stressor in neonatal rats, results in significant deficits of hippocampal function, but these are apparent already in young adults ( Huot et al., 2002). The hippocampus is critical for various types of memory ( Hollup et al., 2001) and is unusually vulnerable to stress ( Bremner et al., 1997 McEwen, 1999 Kim and Diamond, 2002 Sapolsky, 2002). Although enduring effects of early-life experience have been studied in animal models ( Meaney et al., 1988 van Oers et al., 1999 Huot et al., 2002 Poeggel et al., 2003), models for delayed consequences of early-life stress on cognitive function, with onset during adulthood, are uncommon. This implies that early-life stress can have effects that (although not necessarily latent) begin to impact neuronal function significantly during adulthood and aging. 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.Įpidemiological and experimental evidence suggest that early-life experience, particularly “social” or “psychological” stress, may predispose to cognitive dysfunction ( Ammerman et al., 1986 Meaney et al., 1988 Kaplan et al., 2001), as well as depression ( Patchev et al., 1997 Sanchez et al., 2001 Heim et al., 2004), that appears much later in life. At the cellular level, disturbances to hippocampal long-term potentiation paralleled the behavioral changes and were accompanied by dendritic atrophy and mossy fiber expansion. 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. 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. ![]() Progressive cognitive deficits that emerge with aging are a result of complex interactions of genetic and environmental factors. ![]()
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