Objective The hippocampus is a key brain region of multimodal information association, which in turn serves as basis of memory buffer.Molecular and cellular modifications induced by neural activity in hippocampal neurons have been extensively demonstrated.However, the consequence of physiological function changes related to these molecular and cellular modifications, which may account for hippocampus-dependent learning and memory, remains unclear.Methods Using in vivo whole-cell patch-clamp recordings from CA1 pyramidal cells of anaesthetized adult rats and mice, we investigate the plasticity of synaptic responses of hippocampal neurons to a memorized cue (flashing of visual stimulation), which was recently presented to the animal (0-7 days before) as the conditioned stimulus (CS) in fear conditioning.Results Without fear conditioning, a small proportion (~32%, n =31 out 96 cells) of CA1 pyramidal cells exhibited significant synaptic responses to the flash stimulation.Interestingly, one day after fear conditioning—paired stimuli of the flash stimulation (CS) and an electric shock (US), all CA1 pyramidal cells were found to be responsive to the memorized flash stimulation.Consistent with the notion of short-term memory engram mediated by the hippocampus, the increase of the proportion of responsive cells disappeared 7 days after fear conditioning.In CA1 specific NR1-subunit knock-out mice, the proportion of responsive cells to the CS was not changed after fear conditioning, indicating the dependence of the fear conditioning-induced synaptic plasticity of CA 1 pyramidal cells on CA1 NMDA receptors.Conclusion Our data show that fear conditioning recruits widespread CA1 neurons to memorize the related cue.This process may result from switch-on of some synaptic connectivity in the CA1 region by activating its NMDA receptors, which in turn complements the short-term information storage in the hippoeampus.