期刊
STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS
卷 9, 期 1, 页码 1-11出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/10253890600678004
关键词
Amygdala; glucocorticoid; glucocorticoid receptor; HPA axis; learning; long term depression
资金
- NIDA NIH HHS [1K12DA14038] Funding Source: Medline
- NIMH NIH HHS [R01MH64457] Funding Source: Medline
It is now well-documented that exposures to uncontrollable ( inescapable and unpredictable) stress in adulthood can have profound effects on brain and behavior. Converging lines of evidence from human and animal studies indicate that stress interferes with subsequent performances on a variety of hippocampal-dependent memory tasks. Animal studies further revealed that stress impedes ensuing induction of long-term potentiation ( LTP) in the hippocampus. Because the hippocampus is important for key aspects of memory formation and because LTP has qualities congruent to an information storage mechanism, it is hypothesized that stress-induced modifications in hippocampal plasticity contribute to memory impairments associated with stress. Recent studies provide evidence that the amygdala, a structure important in stress- and emotion-related behaviors, plays a necessary role in the emergence of stress-associated changes in hippocampal LTP and memory. Early life stress also alters hippocampal plasticity and memory in a manner largely consistent with effects of adult stress exposure. This review focuses on endocrine-system-level mechanisms of stress effects in the hippocampus, and how stress, by altering the property of hippocampal plasticity, can subsequently influence hippocampal memory.
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