| 1. Ctr. for Neural Sci., New York Univ, New York, NY, USA |
| 2. Lab Neuroendocrinol, Rockefeller Univ, New York, NY, USA |
|
Reactivation of a consolidated fear memory renders it temporarily
vulnerable to disruption by intra-amygdala protein synthesis inhibition.
Stress is known to alter the acquisition, consolidation, and expression
of conditioned fear, but the effects of stress on fear memory reconsolidation
have not been tested. Rats that had previously undergone auditory fear conditioning
(5 tone-footshock pairings) were assigned to pre-reactivation stress, post-reactivation
stress, or a control group. Rats in each of the stress groups were restrained
in wire mesh pouches for 1 hr. Controls were briefly handled in a separate
room. Fear reactivation involved a single re-exposure to the tone conditioned
stimulus in the training context. Restraint stress was given 100 min before
or immediately after reactivation. Tone-elicited freezing was measured in
a separate context 24 hr after reactivation. Pre-reactivation, but not post-reactivation,
restraint stress significantly enhanced conditioned freezing in the test.
Hypothalamic-pituitary-adrenal (HPA) axis suppression with dexamethasone
(25  g, sc, 4 hr before stress) had no effect. However,
blockade of CRF receptors with alpha-helical CRF (20 g, icv, 15 min before
stress) reversed the stress-induced enhancement of reconsolidation without
blocking reconsolidation. Thus, acute restraint stress enhances the reconsolidation
of fear memory through a mechanism that depends on stress-induced activation
of brain CRF receptors, but occurs independently of the HPA axis.
Support Contributed By: R37 MH38774, P50 MH58911, K05 MH067048, I/77376,
HFS-RGP0094
Program No. 208.4
Poster presentation:Sunday, Oct. 24, 11:00 AM - 12:00 PM
Location: NN19 |
