PubMed · 12465682
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Ennio De Renzi. 2002. What does psychogen mean?. https://doi.org/10.1016/s0010-9452(08)70036-4
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Two experiments examined the contribution of the perirhinal cortex (PRh) to retrograde memory for the location of a platform in a water maze. In a previous study, we found that electrolytic lesions of the PRh produced retrograde amnesia, without a temporal gradient, for water-maze problems acquired 4 weeks and 2 days before surgery [Behav. Brain. Res. 114 (2000) 119]. In Experiment 1, we used the same mixed design as in our previous report (time of learning was a within-subjects factor), but PRh lesions were made by aspiration. Contrary to our earlier report, these PRh rats displayed good retention of both platform locations. Combined, these findings indicate that the lesion method may contribute importantly to the pattern of deficits observed. Experiment 2 was conducted similar to Experiment 1, except that a completely between-subjects design was used (time of learning was a between-subjects factor). Rats that received PRh lesions approximately 2 days after the last training session displayed impaired retention of the platform's location, whereas rats that received PRh lesions 4 weeks after training did not. This finding of a temporally graded retrograde amnesia is consistent with our earlier report, and further suggests that the involvement of the PRh in the retention of water-maze problems is time-limited. However, also consistent with our earlier report, the PRh-lesioned rats in Experiment 2 that displayed a retention deficit rapidly reacquired the task. This finding, combined with the negative findings in Experiment 1, suggests that the contribution of the PRh to retrograde memory for platform locations is subtle and may not be due to impaired spatial memory abilities. Additionally, the conflicting results of Experiments 1 and 2 underscore the importance of the design employed in studies of retrograde amnesia in animals.
Lesions of the frontotemporal region of the amygdala, which includes lateral and basal nuclei, cause a loss of conditional fear responses, such as freezing, even when the lesions are made over a year and a half from the original training. These amygdala-damaged animals are not hyperactive and show normal reactivity to strong stimuli such as bright lights. After receiving tone-mild shock pairings rats normally display an appropriately weak response when exposed to the tone. Rats' fear of the tone can be inflated by giving them exposure to strong shocks in the absence of the tone between training and testing. This inflation of fear memory is abolished if the frontotemporal amygdala is inactivated by muscimol only during the inflation treatment with strong shocks. Based on such findings we suggest that the frontotemporal amygdala permanently encodes a memory for the hedonic value of the aversive stimulus used to condition fear.
Cellular theories of memory consolidation posit that new memories require new protein synthesis in order to be stored. Systems consolidation theories posit that the hippocampus has a time-limited role in memory storage, after which the memory is independent of the hippocampus. Here, we show that intra-hippocampal infusions of the protein synthesis inhibitor anisomycin caused amnesia for a consolidated hippocampal-dependent contextual fear memory, but only if the memory was reactivated prior to infusion. The effect occurred even if reactivation was delayed for 45 days after training, a time when contextual memory is independent of the hippocampus. Indeed, reactivation of a hippocampus-independent memory caused the trace to again become hippocampus dependent, but only for 2 days rather than for weeks. Thus, hippocampal memories can undergo reconsolidation at both the cellular and systems levels.