Abstract
J. C. Biedenkapp and J. W. Rudy (2004) reported that the protein synthesis inhibitor anisomycin administered into the hippocampus after context preexposure or contextual fear conditioning impaired subsequent retention performance. In contrast, anisomycin administered after context memory retrieval did not impair subsequent contextual fear conditioning. Their findings challenge the hypothesis that memory retrieval induces memory reconsolidation and suggest that the hypothesis needs to be constrained to account for negative findings. However, their evidence does not suggest compelling clues to how the hypothesis might be constrained to accommodate the findings. Thus, it is not yet clear whether their findings can be explained by a revised reconsolidation hypothesis, or whether some other hypothesis is required to account for postretrieval memory impairment, when it is observed.