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By a dominant account, memory is composed of multiple storage systems, each operating according to unique principles. By an alternative account, memory is a single storage system and operates according to a single set of principles. Selective memory impairments in amnesia serve as the primary evidence for the multiple-system perspective. This thesis reports a critical appraisal of the multiple-system perspective using a combination of computational and empirical methods. In the computational analysis, I adopt the Holographic Exemplar Model, a single-system model of memory based on Hintzman’s (1986) classic MINERVA2 model. I simulate amnesia by manipulating the quality with which items are encoded in memory. In the empirical analysis, I simulate amnesia by manipulating peoples’ quality of encoding by limiting the time given to study stimuli. Simulations 1-2 and Experiments 1-2 simulate a dissociation between classification and recognition. All four analyses are consistent with the original results. Simulation 3 and Experiment 3 simulate single and double dissociations between tachistoscopic identification and recognition. The analyses were consistent with the single but not double dissociation. Simulation 4 and Experiment 4 simulate a dissociation among word-stem completion, cued recall, and recognition. Both analyses were only partially consistent with the original results, representing a failure overall. Simulation 5 and Experiment 5 derived a novel prediction from artificial grammar learning, predicting a non-dissociation between string completion and recognition. The mixed results provide some support for a single-system account of memory and opens opportunities for future work. I argue that the analysis is best considered in convergence with previous work moving toward a more integrated account of memory / February 2017

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Memory refers to the retention of learned information or experiences in the brain. It is known that interference of certain brain functions immediately after training or memory reactivation can cause memory loss (i.e. amnesia). The post-training process is called consolidation and the post reactivation process is called reconsolidation. However, it remains unclear as to: (1) whether appetitive, goal-directed memories undergo reconsolidation, (2) whether overtrained memories undergo reconsolidation, (3) what the nature of amnesia is (i.e. whether it represents storage or retrieval impairment), (4) how to test the nature of amnesia, and (5) whether the brain uses the same mechanism for a new learning and from a second learning. This thesis, composed of five manuscripts, aims to answer these questions. In the first manuscript, the model of incentive learning of appetitive outcomes in instrumental conditioning was used. Protein synthesis inhibitor (PSI) was infused into lateral and basal amygdala (LBA) after the new incentive learning and after the reactivation of the memory. The results show that appetitive memories in controlling goal-directed behaviors underwent consolidation and reconsolidation in the LBA. In the second manuscript, rats were overtrained with auditory fear conditioning and received intra-LBA PSI infusions after memory reactivation. The results show that only old, but not recent, overtrained auditory fear memories underwent reconsolidation. This suggests overtraining sets a boundary condition on memory reconsolidation. Further results showed dorsal hippocampus and intra-LBA NR2B-subunit containing N-methyl-D-aspartic acid receptors (NMDAr) were involved in this boundary condition. In the third manuscript, the unresolved debate about the nature of amnesia was reviewed from a historical perspective and the suggestions on reconciling this issue are proposed. In the fourth manuscript, a new approach was used to test the nature of amnesia in contextual fear conditioning. Because NMDAr blockade impairs a new learning but not a second learning, it is predicted that if a memory is not stored then the second learning should be impaired by NMDAr blockade. The results suggest amnesia of contextual fear memory caused by intra-dorsal hippocampus (dH) PSI infusion represents a storage impairment which gives a different result from extinction induced irretrievability. In the fifth manuscript , the aim is to identify the brain mechanism for the second learning as the previous manuscript suggests it is different from the first learning mechanism. The results show that the first, but not the second learning required voltage-dependent calcium channels and activation in dH. The second learning was impaired by intra-dH or ventral hippocampus (vH) inactivation only when the protein synthesis in the other portion of hippocampus was blocked after training. This suggests while the first learning by default requires dH, the second learning can be acquired through a functional dH or vH. In summary, this thesis extends memory research from consolidating a new learning to characterizing the reconsolidation of appetitive and overtrained memory to consolidating a second learning which will lead to a more complete description of memory process.

Extensive neural connections between the anterior thalamic nuclei (ATN) and the hippocampal system may explain the overlapping amnesic syndromes associated with diencephalic and medial temporal lobe brain injury. Despite the debilitating nature of the diencephalic amnesia, treatments for this condition are lacking. In rats, lesions to the ATN or hippocampus generally produce similar memory deficits, which further implicate these structures in a single functional memory system. First evidence is presented here that seemingly permanent and robust spatial working memory deficits seen after lesions to the ATN in rats are ameliorated by environmental intervention and pharmacological treatment. Post-operative housing of ATN-lesioned rats for 30 days in enriched environment resulted in marked improvements in performance on the spatial working memory task in the cross-maze irrespective of whether rats were exposed to enrichment immediately after surgery or enrichment was delayed by 40 days post-surgery. Long-term beneficial effects of enrichment were also demonstrated. Behavioural improvements were observed when Cerebrolysin - a neurotrophic compound - was injected intraperitoneally for 30 days post-surgery. The combination of enrichment and Cerebrolysin treatment was more effective in inducing recovery on a delayed memory test in the cross-maze task. The influence of enrichment and Cerebrolysin on the neural changes produced by ATN lesions was examined utilising an immediate early gene marker c-fos. Replicating previous studies, ATN lesions produced marked hypoactivity in the retrosplenial cortex, but this effect was not reversed by either enrichment or Cerebrolysin. Unexpectedly, enrichment produced further hypoactivation in this region. Although lesion-induced deficits in a radial-arm maze spatial discrimination task were not improved by enrichment, a related study in our laboratory showed that spatial reference memory can also be improved by enrichment in ATN rats. The current research provides strong support for potential opportunities for therapeutic intervention in the human domain.

Thesis (Ed.D.)--University of Tulsa, 1969. / Bibliography: leaves 41-45.

Thesis (Ph. D.)--University of Washington, 1998. / Vita. Includes bibliographical references (leaves [90]-103).

Treatments such as electroconvulsive shock (ECS) impair later performance of learned responses if presented shortly after learning, but not if delayed for a sufficient time. These gradients are frequently termed retrograde amnesia and interpreted as reflecting a memory consolidation process. The present investigation was concerned with the relationship of the length of the gradient produced by a single ECS to the duration of the memory consolidation process. In the first experiment, rats were trained on a one-trial passive avoidance task and then presented with one of three ECS treatments. The treatments were five ECSs of 0.5 seconds duration spaced either 1 minute apart, 5 seconds apart, or in one continuous 2.5 second duration burst. The five ECSs spaced 1 minute apart were found to impair performance when presented immediately, 1 hour, 24 hours, and 48 hours but not 9 days after passive avoidance training. Five ECSs spaced 5 seconds apart impaired performance when presented immediately or 1 hour but not 24 hours after training. In contrast, the single 2.5 second duration ECS impaired performance when presented immediately but not 1 hour or longer after training. The impairments produced by the five ECSs spaced 1 minute apart at 1 hour and 24 hours were found to be permanent over 11 days. The second experiment examined whether the long gradient produced by five ECSs spaced 1 minute apart was qualitatively different from single ECS gradients. Five ECSs spaced 1 minute apart were presented following passive avoidance training to rats anesthetized with ether or sodium pentobarbital. In both cases, the series of ECSs still impaired performance when presented 1 or 24 hours but not 9 days following passive avoidance training. This finding does not provide support for a distinction between the gradients produced by a single ECS and a series of ECSs. These results were therefore interpreted as showing that the length of the gradient produced by a single ECS in a passive avoidance task is not a good estimate of the duration of time required for memory consolidation. In this passive avoidance task, consolidation appears to continue for a period of at least several days, while the gradient produced by a single ECS was less than 1 hour. In the third experiment, rats were trained on a one - trial appetitive taste and then presented with either five ECSs spaced 1 minute apart, or a single ECS of 0.5 seconds or 2.5 seconds duration. In contrast to the results in the passive avoidance task, the five ECSs paced 1 minute apart did not produce a longer gradient than a single ECS of either 0.5 or 2.5 seconds duration. All three treatments impaired performance when presented 15 seconds but not 1 hour after training. Several possible explanations for the different effects of the series of ECSs in the two tasks are considered, and it is concluded that this difference probably reflects differences between the memory consolidation processes in the two tasks. / Arts, Faculty of / Psychology, Department of / Graduate

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