Characterization of fear memory reconsolidation - PubMed (original) (raw)
Characterization of fear memory reconsolidation
Sevil Duvarci et al. J Neurosci. 2004.
Abstract
Reactivation of consolidated memories returns them to a protein synthesis-dependent state. One interpretation of these findings is that the memory reconsolidates after use. Two alternative interpretations are that protein synthesis inhibition facilitates extinction and that postreactivation protein synthesis inhibition leads to an inability to retrieve the consolidated memory. First, using two different approaches, we report that reconsolidation cannot be reduced down to facilitated extinction. We show that the reconsolidation deficit does not show renewal after a contextual shift, whereas an extinguished auditory fear memory does under the same conditions and the deficit occurs regardless of whether the memory is reactivated with an extinction [conditioned stimulus (CS) alone] or a reinforced trial (CS-unconditioned stimulus). To address the issue of whether postreactivation anisomycin leads to an inability to retrieve the consolidated memory, we used two traditional assays for retrieval deficits. First, we demonstrate that the amnesia induced by blockade of reconsolidation does not show any spontaneous recovery. Second, we show that application of reminder shock does not result in the reinstatement of the memory. These findings support the idea that reactivation of consolidated memories initiates a second time-dependent memory formation process.
Figures
Figure 1.
The impairment induced by postreactivation anisomycin infusions is not context specific. a, The behavioral procedure used for experiment 1. b, Anisomycin groups were impaired in the PR-LTM test. The first word in the group name refers to whether animals received anisomycin or ACSF infusions. The second word refers to whether they will be tested in the same (Same) or different (Diff) context.
Figure 3.
Consolidated memories that are reactivated by a reinforced trial are sensitive to protein synthesis inhibition. a, The behavioral procedure used for experiment 2. Vertical open-headed arrows represent intra-LBA infusions in all figures. b, The first and second letter of the group name refer to the treatment received (A, anisomycin; V, vehicle ACSF) after the first and second training trial, respectively. The score of animals in group V/A sharply declined between day 2 and the final test. This is consistent with the predictions of reconsolidation but not consolidation.
Figure 2.
a, Schematic representation of the amygdala at four different rostrocaudal planes. The numbers represent the posterior coordinate from bregma. Injector placements in the LBA are represented by the filled symbols; black filled squares represent Aniso/Different group placements, gray filled circles represent anisomycin/Same group placements. The placements for the other groups in this experiment and subsequent experiments all demonstrate similar distributions and therefore are not shown. b, Photomicrographs of representative cannula placements (white square) in the BLA. The left photomicrograph is taken from an animal that received vehicle, and the right is from an animal that received anisomycin. LA, Lateral nucleus; B, basal nucleus; CE, central nucleus.
Figure 4.
The amnesia resultant from anisomycin infusions does not show spontaneous recovery over 24 d. a, Schematic of behavioral procedure used. b, Anisomycin infusions impaired PR-LTM but had no effect on PR-STM. Twenty-four days after reactivation, anisomycin rats were still impaired.
Figure 5.
The amnesia resultant from anisomycin infusions does not show reinstatement. a, Schematic of behavioral procedure used. Vertical open-headed arrows represent intra-LBA infusions in all figures. b, Anisomycin infusions impaired PR-LTM. Animals did not recover from this deficit with a noncontingent footshock. c, After retraining, the freezing scores of the anisomycin rats were comparable with their reactivation score, demonstrating that they have a functional amygdala.
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