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The Journal of Neuroscience, July 15, 2001, 21(14):5222-5228
Amygdala Is Critical for Stress-Induced Modulation of Hippocampal
Long-Term Potentiation and Learning
Jeansok J.
Kim1,
Hongjoo J.
Lee1,
Jung-Soo
Han2, and
Mark G.
Packard1
1 Department of Psychology, Yale University, New Haven,
Connecticut 06520-8205, and 2 Department of Psychology,
Johns Hopkins University, Baltimore, Maryland 21218
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
long-term 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.
Key words:
hippocampus; learning; fear; emotion; glucocorticoids; corticosterone; synaptic plasticity
Copyright © 2001 Society for Neuroscience 0270-6474/01/21145222-07$05.00/0
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