Memory

Summary

Memory is the faculty of the mind by which data or information is encoded, stored, and retrieved when needed. It is the retention of information over time for the purpose of influencing future action. If past events could not be remembered, it would be impossible for language, relationships, or personal identity to develop. Memory loss is usually described as forgetfulness or amnesia. Memory is often understood as an informational processing system with explicit and implicit functioning that is made up of a sensory processor, short-term (or working) memory, and long-term memory. This can be related to the neuron. The sensory processor allows information from the outside world to be sensed in the form of chemical and physical stimuli and attended to various levels of focus and intent. Working memory serves as an encoding and retrieval processor. Information in the form of stimuli is encoded in accordance with explicit or implicit functions by the workin

Official source

https://en.wikipedia.org/wiki/Memory

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Video Prediction Recalling Long-term Motion Context via Memory Alignment Learning

Hakgu Kim

Our work addresses long-term motion context issues for predicting future frames. To predict the future precisely, it is required to capture which long-term motion context (e.g., walking or running) the input motion (e.g., leg movement) belongs to. The bottlenecks arising when dealing with the long-term motion context are: (i) how to predict the long-term motion context naturally matching input sequences with limited dynamics, (ii) how to predict the long-term motion context with high-dimensionality (e.g., complex motion). To address the issues, we propose novel motion context-aware video prediction. To solve the bottleneck (i), we introduce a long-term motion context memory (LMC-Memory) with memory alignment learning. The proposed memory alignment learning enables to store long-term motion contexts into the memory and to match them with sequences including limited dynamics. As a result, the long-term context can be recalled from the limited input sequence. In addition, to resolve the bottleneck (ii), we propose memory query decomposition to store local motion context (i.e., low-dimensional dynamics) and recall the suitable local context for each local part of the input individually. It enables to boost the alignment effects of the memory. Experimental results show that the proposed method outperforms other sophisticated RNN-based methods, especially in long-term condition. Further, we validate the effectiveness of the proposed network designs by conducting ablation studies and memory feature analysis. The source code of this work is available(dagger).

IEEE COMPUTER SOC2021

Learning and memory rely on synaptic communication in which intracellular signals are transported to the nucleus to stimulate transcriptional activation. Memory induced transcriptional increases are accompanied by alterations to the epigenetic landscape and can be pharmacologically mimicked to ameliorate memory in both healthy and cognitively impaired animals. Of particular interest in this regard is histone acetylation, as this epigenetic modification is enriched during memory formation and is readily amenable to pharmacological manipulation by means of histone deacetylase inhibitors (HDACis). Although multiple studies have shown that systemic HDACi administration can improve memory formation, their mode of action is not yet fully understood. In this study, we tested whether HDACis â given systemically â augment epigenetic, transcriptional and electrophysiological responses that are induced by learning, thus amplifying naturally occurring responses via cognitive epigenetic priming. To do this, we combined a system-wide HDACi treatment with a sub-threshold contextual fear conditioning (CFC) paradigm, a weakened Pavlovian modal that, alone, does not lead to long term memory formation. We found that, in combination, HDACi and CFC improve recent contextual memory that is accompanied by enhanced long-term potentiation in the hippocampus. Conversely, combined HDACi-CFC treatment induced no such synaptic strengthening in the striatum, a brain region that is not directly activated by fear conditioning. We then used bulk and single nuclear RNA-sequencing to show that HDACi activates unique transcriptional pathways, both between the two brain regions and between cell types within the hippocampus, indicating that HDACi does not act indiscriminatingly, but instead supports cellular processes that are already occurring in response to the conditioning. Finally, we show that HDACi treatment paired with contextual fear conditioning enriches H3K27ac at enhancers of known memory-related genes within the hippocampus but that not all these genes are necessarily more transcriptionally active at the same time point. These results indicate that systemic HDACi administration acts as a cognitive enhancer by amplifying brain-region specific processes that are naturally induced during memory formation but that these results may not be a direct effect of enhancer histone acetylation. These findings shed light on the mechanisms of HDACi-mediated cognitive epigenetic priming and help to pave the way for potential new therapies for memory-related disorders.

EPFL2022

Stress at learning facilitates memory formation by regulating AMPA receptor trafficking through a glucocorticoid action

Lisa Conboy, Maria del Carmen Sandi Perez

Stress and glucocorticoids (GCs) can facilitate memory formation. However, the molecular mechanisms mediating their effects are largely unknown. alpha-Amino-3-hydroxy-5- methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR) trafficking has been implicated in the changes in synaptic strength at central glutamatergic synapses associated with memory formation. In cell cultures, corticosterone has been shown to condition the synaptic trafficking of the AMPAR GluA2 subunit. In this study, we investigated the involvement of GluA2 trafficking in the facilitation of learning by stress. Using the water maze spatial task involving different stress levels, mice trained under more stressful conditions (water at 22 degrees C) showed better learning and memory, and higher post-training corticosterone levels, than mice trained under lower stress (water at 30 degrees C). Strikingly, this facilitated learning by stress was accompanied by enhanced synaptic expression of GluA2 AMPARs that was not observed in mice trained under less stressful conditions. Interfering with GC actions by injecting the GC synthesis inhibitor, metyrapone, blocked both the memory facilitation and the enhanced GluA2 trafficking induced by stressful learning. Intracerebroventricular infusion of the peptide, pep2m, that blocks GluA2 synaptic trafficking by interfering with the interaction between N- ethylmaleimide-sensitive factor and GluA2, impaired immediate performance at learning as well as long-term memory retrieval, supporting a causal role for GluA2 trafficking in stress-induced facilitation of spatial learning and memory. Evidence for the involvement of the neural cell adhesion molecule N-cadherin in interaction with GluA2 is also provided. These findings underscore a new mechanism whereby stress can improve memory function.Neuropsychopharmacology advance online publication, 4 November 2009; doi:10.1038/npp.2009.172.

Nature Publishing Group2010

Stress at learning facilitates memory formation by regulating AMPA receptor trafficking through a glucocorticoid action

Lisa Conboy, Maria del Carmen Sandi Perez

Nature Publishing Group2010

EPFL2022