Retrieval of contextual fear memory by re-exposure to conditioned stimulus (CS; context) initiates gene expression-dependent processes; reconsolidation and extinction. Previous our study showed that short (3 min) re-exposure to the CS inducing memory reconsolidation activated gene expression in the hippocampus and amygdala, while long (30 min) re-exposure inducing memory extinction activated it in the medial prefrontal cortex and amygdala (Mamiya et al, 2009). Poly (ADP-ribose) polymerase-1 (PARP-1) has been known to covalently modify nuclear proteins including histones and transcription factors through poly ADP-ribosylation. Interestingly, recent studies have suggested that poly ADP-ribosylation by PARP-1 plays critical roles in long-term neuronal plasticity and formation of long-term memory. To understand roles of poly ADP-ribosylation in the regulation of contextual fear memory after retrieval, we have examined effects of inhibition of poly ADP-ribosylation in the hippocampus and medial prefrontal cortex in reconsolidation and extinction. Mice were micro-infused a PARP-1 inhibitor (3-aminobenzamide (3AB) or PJ34) into the hippocampus or medial prefrontal cortex 5 min before or immediately after the re-exposure for 3 or 30 min. This inhibition of poly ADP-ribosylation in the hippocampus impaired reactivated contextual fear memory when tested 24 hrs, but not 2 hrs, after the re-exposure for 3 min, suggesting that poly ADP-ribosylation in the hippocampus is required for reconsolidation of contextual fear memory. Additionally, the inhibition of poly ADP-ribosylation in the medial prefrontal cortex, but not the hippocampus, blocked long-term extinction of contextual fear memory, suggesting that poly ADP-ribosylation in the medial prefrontal cortex is required for consolidation of extinction memory. Our findings suggest that poly ADP-ribosylation in the hippocampus and medial prefrontal cortex plays essential roles in reconsolidation and extinction, respectively, of contextual fear memory.