Long-lasting hippocampal potentiation and contextual memory consolidation

In order to ascertain whether there are hippocampal electrophysiological modi®cations speci®cally related to memory, exploratory activity and emotional stress, extracellular electrical activity was recorded in hippocampal slices prepared from the brains of male adult rats. Several groups of animals were employed: (i) rats which had freely explored the experimental apparatus (8 min exposure); (ii) rats which had been subjected, in the same apparatus, to a fear conditioning paradigm training entailing the administration of aversive electrical footshocks (8 min exposure); (iii) rats to which the same number of aversive shocks had been administered in the same apparatus, but temporally compressed so as to make dif®cult the association between painful stimuli and the apparatus (30 s exposure); (iv) naõÈve rats never placed in the apparatus. Half of the rats from each treatment group were used for retrieval testing and the other half for hippocampal excitability testing. The conditioned freezing response was exhibited for no less than 4 weeks. Hippocampal excitability was measured by means of input±output curves (IOC) and paired-pulse facilitation curves (PPF). Retrieval testing or brain slices preparation were performed at increasing delays after the training sessions: immediately afterwards or after 1, 7 or 28 days. Only the rats subjected to the fear conditioning training exhibited freezing when placed again in the apparatus (retrieval testing). It was found that IOCs, with respect to naõÈve rats, increased in the conditioned animals up to the 7-day delay. In free exploration animals the IOCs increased only immediately after the training session. In all other rats no modi®cation of the curves was observed. IOC increases do not appear to imply presynaptic transmitter release modi®cations, because they were not accompanied by PPF modi®cations. In conclusion, a clearcut correlation was found between the increase in excitability of the Schaffer collateral±CA1 dendrite synapses and freezing response consolidation.