Introduction: Gap junctions are specialized cell–cell contacts between eukaryotic cells through which they communicate. This type of communication has the potential to modulate memory process. We evaluated the effects of the gating of the hippocampal CA1 area gap junction channels on memory consolidation, using passive avoidance task. Materials and Methods: 72 adult male Wistar rats were distributed into 9 groups of 8 each. Two guiding cannulas were bilaterally implanted in the hippocampal CA1 area of all rats. One week after surgery, the animals received an electrical shock with the intensity and duration of 0.3 mA and 1s, respectively. Immediately after training 25, 75 or 150 nM doses of carbenoxolone, a non-selective blocker of gap junction channels or 50, 150 and 1500 nM doses of trimethylamine, an opener of gap junction channels were injected. Another group received 50 nM trimethylamine and 10 min later 75 nM carbenoxolone, immediately post-training. 24 hours later, memory retrieval was assessed. Results: Post-training injection of carbenoxolone significantly and dose- dependently decreased step-through latency, whereas post-training injection of trimethylamine showed a tendency toward increasing step-through latency. Post-training injection of trimethylamine (50 nM) increased step-through latency, significantly compared with post-training injection of carbenoxolone (75 nM and 150 nM). Post-training injection of trimethylamine (50 nM) before carbenoxolone (75 nM) reversed the effects of carbenoxolone on inhibition of memory consolidation. Conclusion: These data suggest that the intercellular coupling via gap junction channels in the hippocampal CA1 cells is crucial for memory consolidation in the passive avoidance task.