期刊
JOURNAL OF NEUROSCIENCE
卷 21, 期 14, 页码 5222-5228出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.21-14-05222.2001
关键词
hippocampus; learning; fear; emotion; glucocorticoids; corticosterone; synaptic plasticity
资金
- NIMH NIH HHS [R29MH56973] Funding Source: Medline
- PHS HHS [P4000 D51-2055] Funding Source: Medline
Stress is a biologically significant factor shown to influence synaptic plasticity and memory functioning in the hippocampus. This study examined the role of the amygdala, a brain structure implicated in coordinating stress behaviors and modulating memory consolidation, in mediating stress effects on hippocampal longterm potentiation (LTP) and memory in rats. Electrolytic lesions of the amygdala effectively blocked the adverse physiological and behavioral effects of restraint and tailshock stress, without impeding the increase in corticosterone secretion to stress. Physiologically, hippocampal slices from stressed animals exhibited impaired LTP relative to slices from unstressed control animals, whereas hippocampal slices from stressed animals with amygdalar lesions exhibited normal LTP. Behaviorally, stressed animals were impaired in retention of a hippocampal-dependent hidden platform version of the Morris water maze task, and this impairment was blocked by amygdalar lesions. In a fixed location-visible platform water maze task that can be acquired by independent hippocampal and nonhippocampal memory systems, stress enhanced the use of nonhippocampal-based memory to acquire the task. These results indicate that an intact amygdala is necessary for the expression of the modulatory effects of stress on hippocampal LTP and memory.
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