Recent studies have shown that reactivated contextual fear memory becomes labile and is re-stabilized through memory reconsolidation that requires CREB-mediated transcription in the hippocampus (HP) (Suzuki et al., 2004; Mamiya et al., 2009). We previously found that short re-exposure to conditioned stimulus (CS; context) for 3 min induced reconsolidation on recent, but not remote, contextual fear memory. Interestingly, we also found that long re-exposure to the CS for 10 min enabled to induce reconsolidation of remote contextual fear memory. In this study, we tried to understand mechanisms by which the stability of remote contextual fear memory is regulated. Mice were trained with a single footshock and re-exposed to training context for 3 or 10 min 1 or 30 days later. To identify which brain regions were activated when remote contextual fear memory is reconsolidated, we first performed immunohistochemistry to measure the expression levels of c-fos, a target gene of CREB. Similarly with our previous finding, re-exposure to CS for both 3 and 10 min 1 day after training led to increase in c-fos expression in the HP. Interestingly, re-exposure to CS for 10 min, but not 3 min, 30 days after training led to increase in c-fos expression in the HP, suggesting that long re-exposure to CS enables to induce gene expression in the HP even when memory is remote. Next, to understand roles of gene expression in the HP following re-exposure to CS in remote contextual fear memory, mice were micro-infused with a protein synthesis inhibitor, anisomycin (ANI) into the HP immediately after re-exposure. ANI treatment disrupted reactivated fear memory in re-exposure to CS for 3 or 10 min 1 and 30 days, respectively, after training, suggesting that gene expression in the HP is required for reconsolidation of both recent and remote contextual fear memory. Our observations suggest that remote contextual fear memory becomes labile following long re-exposure to CS and then is reconsolidated through gene expression in the HP.