Recognition memory which requires judgements to be made about the prior occurrence of stimuli or groups of stimuli has been shown to depend upon the integrity of the perirhinal cortex. For example, electrophysiological recording experiments have revealed that changes in the responses of neurones in the perirhinal cortex are central to the ability to judge prior occurrence. Further ablation of perirhinal cortex has been shown to produce significant impairments in memory tasks requiring the ability to discriminate between novel and familiar stimuli. Our research into the neural basis of recognition memory has focussed on exploring the hypothesis that changes in synaptic efficacy (exemplified by long term potentiation (LTP) and long term depression (LTD)) underlie the familiarity discrimination processes. To achieve this aim our strategy has been to manipulate specific receptors or signalling pathways in the perirhinal cortex and to compare the results of such manipulations across different levels of experimental analysis (cellular, systems and behavioural). I shall present recent data from our laboratory showing that pharmacological blockade of ionotropic and metabotropic glutamate receptors in the perirhinal cortex impairs both familiarity discrimination and the induction of long-term synaptic plasticity in the perirhinal cortex. I shall also present data from experiments in which we have used viral vectors which encode a dominant negative form of CREB to block CREB-mediated transcription in the perirhinal cortex. This transduction resulted in both a behavioural impairment in object recognition memory and a failure in the maintenance of LTP in perirhinal slices. Together these results suggest that the mechanisms which underlie synaptic plasticity may provide candidate mechanisms for processes effecting recognition memory.