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Glucocorticoid involvement in memory formation in a rat model for traumatic memory
M Isabel Cordero1, Nyika D Kruyt, J Joaquin Merino
1Department of Psychobiology, Universidad Nacional de Educacion a Distancia, Ciudad Universitaria s/n, 28040 Madrid, Spain.
Stress (Amsterdam, Netherlands)
|August 13, 2002
Summary
Inhibiting glucocorticoid synthesis with metyrapone before training reduced traumatic memory formation in rats, regardless of stressor intensity. This highlights glucocorticoids
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Endocrinology
Background:
- Contextual fear conditioning with high stress is a model for traumatic memory.
- Glucocorticoids influence memory strength, but their role during high-stress training is unclear.
- Glucocorticoid receptor antagonist effects varied with stressor intensity.
Purpose of the Study:
- To investigate if inhibiting glucocorticoid synthesis during training affects contextual fear conditioning under different stressor intensities.
- To determine the role of glucocorticoid synthesis inhibition in modulating traumatic memory formation.
Main Methods:
- Rats received metyrapone (a glucocorticoid synthesis inhibitor) before contextual fear conditioning at moderate (0.4 mA) or high (1 mA) shock intensities.
- Long-term fear memory expression and plasma corticosterone levels were assessed.
Main Results:
- Metyrapone dose-dependently attenuated long-term contextual fear conditioning in both moderate and high shock intensity groups.
- Metyrapone effectively prevented the rise in plasma corticosterone levels post-training.
- Glucocorticoid synthesis inhibition impacted memory consolidation irrespective of stressor intensity.
Conclusions:
- Glucocorticoids play a crucial role in the formation of traumatic memories.
- Interfering with glucocorticoid synthesis during training can modulate memory consolidation.
- These findings support the involvement of glucocorticoids in traumatic memory consolidation.