Mechanisms of Late-Onset Cognitive Decline after Early-Life Stress
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| Názov: | Mechanisms of Late-Onset Cognitive Decline after Early-Life Stress |
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| Autori: | Kramár, E, Baram, TZ, Brunson, KL, Lynch, G, Yanagihara, TK, Colgin, LL, Lin, B, Chen, Y |
| Zdroj: | The Journal of neuroscience : the official journal of the Society for Neuroscience, vol 25, iss 41 |
| Informácie o vydavateľovi: | Society for Neuroscience, 2005. |
| Rok vydania: | 2005 |
| Predmety: | Male, 0301 basic medicine, Time Factors, Long-Term Potentiation, psychology, In Vitro Techniques, Stress, Hippocampus, References (75) View In Table Layout, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Animals, Cognition Disorders: physiopathology, Psychological: physiopathology, Age of Onset, Maternal Behavior, Age Factors, Long-Term Potentiation: physiology, Rats, Hippocampus: physiology, Maternal Behavior: physiology, Female, Sprague-Dawley, Cognition Disorders, Stress, Psychological |
| Popis: | 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. |
| Druh dokumentu: | Article |
| Popis súboru: | application/pdf |
| Jazyk: | English |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.2281-05.2005 |
| Prístupová URL adresa: | http://www.jneurosci.org/content/25/41/9328.full.pdf https://pubmed.ncbi.nlm.nih.gov/16221841 https://www.jneurosci.org/content/25/41/9328 https://escholarship.org/uc/item/02k3375k.pdf https://escholarship.org/content/qt02k3375k/qt02k3375k.pdf?t=nin4dy http://hub.hku.hk/handle/10722/90951 http://europepmc.org/articles/PMC3100717 http://www.jneurosci.org/content/25/41/9328.full https://escholarship.org/uc/item/02k3375k http://hdl.handle.net/10722/90951 |
| Rights: | CC BY NC SA |
| Prístupové číslo: | edsair.doi.dedup.....3876d9da3e711d849a2268f43758806b |
| Databáza: | OpenAIRE |
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Nájsť tento článok vo Web of Science | Abstrakt: | 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. |
|---|---|
| ISSN: | 15292401 02706474 |
| DOI: | 10.1523/jneurosci.2281-05.2005 |