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New, Forgotten, and Savings Memory for Long-Term Sensitization in Aplysia Pleural Ganglia

ABSTRACT: We used a custom-designed microarray to characterize the transcriptional response that accompanies longt-term sensitization training in the marine mollusk Aplysia californica. We characterized transcription for a new memory (1 day after training), a forgotten memory (8 days after training) and for a long-term savings memory (8 days after training but 1 day after a reminder that re-instates the sensitization memory). All animals received a 1-day unilateral LTS training protocol (4 rounds of noxious shock at 30 min intervals, each shock 10s of 1/2s off 1/2on 90mA 60-hz biphasic square-wave shock). This produced robust sensitization in all animals (measured as an increase in T-SWR response from baseline to 24h after training). In the forgetting condition, animals received training on day 1, and post-tests on days 7 and 8 showed little-to-no evidence of recall (T-SWR responses on the trained side returned to close to baseline). In the savings condition, animals received training on day 1 that produced strong sensitization, showed forgetting on day 7, and then received a weak bilateral shock as a reminder (day 7), producing a long-term savings memory on day 8 (a re-instatement of the behavioral expression of sensitization on the previously trained side). In the new memory condition, animals received sham training on day 1, then real training on day 7, producing robust sensitization measured on day 8. Pleural ganglia were harvested on day 8. Samples from a left-trained and right-trained animal were combined to smooth out lateralized gene expression. The pleural ganglia contains the VC nociceptors, which are thought to play a primary role in expressing LTS memory.

ORGANISM(S): Aplysia californica

PROVIDER: GSE152045 | GEO | 2020/06/09

REPOSITORIES: GEO

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Project description:A fundamental question in neuroscience is how memories are stored and retrieved in the brain. Many neurological, psychiatric and neurodevelopmental disorders are associated with cognitive deficits. Therefore characterizing the biological basis of these processes is critical for understanding normal and abnormal brain function. It is known that long-term memory formation requires transcription and translation as well as epigenetic processes that control gene expression. In this study we examined genome-wide gene expression changes during memory consolidation and after memory retrieval. We observe the largest changes in gene expression 30 minutes after memory acquisition and retrieval, and several novel genes were found to be affected by both. Interestingly, acquisition and retrieval of memory down-regulate different processes. Chromatin assembly is down-regulated after memory acquisition whereas RNA processing is down-regulated so after retrieval. Histone variant H2AB levels are reduced following acquisition, while splicing factor Rbfox1 and NMDA receptor-dependent microRNA miR-219 are down-regulated following retrieval. We also show that miR-219 down-regulation after retrieval is accompanied by up-regulation of its target protein CAMKIIÎ³. Our study highlights for the first time the differential involvement of epigenetic mechanisms that control gene expression, such as histone variants and post-transcriptional RNA processing, during memory acquisition and retrieval. 72 total samples were analyzed, including animals trained in a contexual conditioning paradigm (FC) and controls. Tissue was collected at 30 minutes (FC30), 4 hours (FC4), 12 hours (FC12) and 24 hours after FC (FC24) as well as 30 minutes after testing for retrieval of the memory (RT30). Testing was performed at 24 hours after training over a 5-minute interval. Animals that were handled but not trained were dissected at the same time of day to control for variations due to circadian rhythms (CC30, CC4 andCC12). The protocol was repeated over the course of 2 weeks to obtain 9 animals (2 hippocampi) per group, so that 9 independent FC experiments were represented in each time point and all animals for each group were dissected at the exactly the same time of day.

Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Experiment Overall Design: Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals (NT, 5D, and 21D, N=10/group). Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal)

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New, Forgotten, and Savings Memory for Long-Term Sensitization in Aplysia Pleural Ganglia

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