Memory Strengthening Research Articles

베트남인 학습자의 한국어 어휘 학습 전략 연구

This study aims to provide research data for effective strategy learning by finding out the frequency of vocabulary learning strategy use and variable-based strategy use aspects in Vietnamese Korean language learners. The study results displayed that Vietnamese Korean language learners employed ‘Discovery Strategies’ more than ‘Consolidation strategies’. Among six sub-strat egies, ‘Cognitive Strategy’, which is a sub-strategy of ‘Discovery Strategies’ was used a lot. When analyzing strategy use aspects depending on learner variables, such as gender, experience with vocabulary learning strategy learning and experience with other foreign language learning, male students showed a higher frequency of strat egy use than female students, but ‘Consolidation strategies’ that is a sub-strategy of ‘Memory Strengthening strategy’ was more used among female students. In relation to experience with vocabulary strategy learning, the use of strategies was bigger when students learned strategies. In relation to experience with other foreign language learning, ‘Decision Strategies’ of ‘Discovery Strategies’ was more used among learners with experience in learning other foreign languages. It is anticipated that this study would provide the direction of Korean vocabulary learning strategy education and implications for rapidly increasing Vietnamese Korean language learners.

Weak cued fear memory strengthening by re-activating the engram

Weak cued fear memory strengthening by re-activating the engram

MEMORY IMPROVEMENT IN THE ELDERLY THROUGH GHUNNAH THERAPY

The vibrations produced by reading ghunnah have a favorable influence on a person's cognitive function, specifically in the form of memory strengthening or improvement in order to prevent senile dementia. The ability of tajweed Ghunnah is thought to have a good impact on memory. Furthermore, this capacity can help to prevent senility, which is a typical problem among the elderly. The purpose of this study was to investigate the effect of ghunnah therapy on memory. The quantitative approaches utilized in this investigation were combined with a pre-post experimental design. The Reading Span Test method was used to assess respondents' memory before and after ghunnah therapy. The goal was to demonstrate that Ghunnah's intervention variable was the only one that had an effect on memory improvement. The findings revealed that respondents' memory scores improved before and after ghunnah therapy. As a result, it is possible to conclude that ghunnah therapy has a substantial association with memory.

The interconnection and function of associative memory neurons are upregulated for memory strengthening.

Memories associated to signals have been proven to rely on the recruitment of associative memory neurons that are featured by mutual synapse innervations among cross-modal cortices. Whether the consolidation of associative memory is endorsed by the upregulation of associative memory neurons in an intramodal cortex remains to be examined. The function and interconnection of associative memory neurons were investigated by in vivo electrophysiology and adeno-associated virus-mediated neural tracing in those mice that experienced associative learning by pairing the whisker tactile signal and the olfactory signal. Our results show that odorant-induced whisker motion as a type of associative memory is coupled with the enhancement of whisking-induced whisker motion. In addition to some barrel cortical neurons encoding both whisker and olfactory signals, i.e., their recruitment as associative memory neurons, the synapse interconnection and spike-encoding capacity of associative memory neurons within the barrel cortex are upregulated. These upregulated alternations were partially observed in the activity-induced sensitization. In summary, associative memory is mechanistically based on the recruitment of associative memory neurons and the upregulation of their interactions in intramodal cortices.

Sleep disruption by memory cues selectively weakens reactivated memories.

A widely accepted view in memory research is that recently stored information can be reactivated during sleep, leading to memory strengthening. Two recent studies have shown that this effect can be reversed in participants with highly disrupted sleep. To test whether weakening of reactivated memories can result directly from sleep disruption, in this experiment we varied the intensity of memory reactivation cues such that some produced sleep arousals. Prior to sleep, participants (local community members) learned the locations of 75 objects, each accompanied by a sound naturally associated with that object. Location recall was tested before and after sleep, and a subset of the sounds was presented during sleep to provoke reactivation of the corresponding locations. Reactivation with sleep arousal weakened memories, unlike the improvement typically found after reactivation without sleep arousal. We conclude that reactivated memories can be selectively weakened during sleep, and that memory reactivation may strengthen or weaken memories depending on additional factors such as concurrent sleep disruption.

A conversion-type lithium artificial synapse with dispersed nano-silica fabricated by UV-curing method

The rapid growth of information puts forward new requirements for computer including denser memory capacity and faster response beyond the traditional von Neumann architecture. One promising strategy is to employ novel computing devices such as artificial synapses (AS). Here, an Au/LPSE-SiO2/Si AS (LPSE-SiO2 AS) with a simple sandwich structure was fabricated by UV curing. LPSE-SiO2 AS emulated synaptic plasticity including excitatory postsynaptic current, paired-pulse facilitation, and spike-dependent plasticity. It also simulated the memory strengthening and forgetting analogue to biological system. The realization of synaptic plasticity is due to the homogeneously dispersed nano-silica in LPSE, which acts as lithium ions trapping center and conducts a reversible electrochemical conversion reaction with Li ions with pulse stimulation. These results indicate the potential for LPSE-SiO2 AS in future large-scale integrated neuromorphic networks.

Pengaruh Nada Suara Pencerita Storytelling dan Gambar Bergerak Pada Media Digital Youtube pada Peningkatan Kemampuan Mengingat Berurutan Peserta Program Sekolahku YKAKI Jakarta

The concept of learning with video aids through the Youtube application is an option in the learning model of the Sekolahku YKAKI (Indonesian Care for Cancer Kids Foundation) program to facilitate memory strengthening by using repeated videos. This research is a qualitative research related to problems with the procedures for collecting data from interviews, observations, and archives. The activity of children watching videos is scheduled to be repeated with the assistance of the teacher, it is hoped that it will provide benefits for improving the memory of both the whole series of stories, as well as some of the details contained in the recordings. This activity is beneficial in the Sekolaku/My School program of YKAKI. Children who participate in Sekolahku/My School program are children with cancer who are undergoing treatment with various methods that consume energy and interfere with learning concentration. Inserting a message through a story using Youtube media which is specially made with the voice of the chosen narrator and equipped with sound effects supporting the story makes this YouTube video an option for memory strengthening in the learning model because there is a dynamic emphasis on the narrator's intonation with structured repetition.

Ghrelin Is Effective on Passive Avoidance Memory by Altering the Expression of NMDAR and HTR1a Genes in the Hippocampus of Male Wistar Rats.

Memory-dependent psychological behaviors have an important role in life. Memory strengthening in adulthood to prevent its defects in aging is a significant issue. The ghrelin endogenous hormone improves memory by targeting glutamatergic and serotonergic circuits. Also, citicoline, a memory strengthening drug in aging, is not recommended to adults due to its side effects. The current study aims to test that ghrelin treatment, like citicoline, would improve passive avoidance memory via expression of the genes encoding the N-methyl-D-aspartate receptor (NMDAR1) and the serotonin receptor 1A (HTR1α) involved in this process. Five groups of adult male rats received (1) saline (as control), (2) 0.5 mg/kg citicoline, or (3-5) 0.3, 1.5, and 3 nmol/μl ghrelin). The rats received the drugs via intra-hippocampal injection. Passive avoidance memory was determined using a shuttle box device. The latency to enter the dark chamber before (IL) and after (RL) injection and the total duration of the animal's presence in the light compartment (TLC) were evaluated. Then, the gene expression rates of NMDAR1 and HTR1α were measured by the Real-Time PCR. Ghrelin and citicoline had some similar and significant effects on passive avoidance memory, and both increased NMDAR1 and decreased HTR1α expression. Ghrelin, like citicoline, improves passive avoidance learning by altering the NMDAR1 and HTR1α expression in the hippocampus.

Subjective feeling of re-experiencing past events using immersive virtual reality prevents a loss of episodic memory.

IntroductionPersonally meaningful past episodes, defined as episodic memories (EM), are subjectively re‐experienced from the natural perspective and location of one's own body, as described by bodily self‐consciousness (BSC). Neurobiological mechanisms of memory consolidation suggest how initially irrelevant episodes may be remembered, if related information makes them gain importance later in time, leading for instance, to a retroactive memory strengthening in humans.MethodsUsing an immersive virtual reality system, we were able to directly manipulate the presence or absence of one's body, which seems to prevent a loss of initially irrelevant, self‐unrelated past events.Results and ConclusionOur findings provide an evidence that personally meaningful memories of our past are not fixed, but may be strengthened by later events, and that body‐related integration is important for the successful recall of episodic memories.

Ejercicio y algunos mecanismos moleculares que subyacen a una mejora del desempeño en tareas cognitivas

Potenciar el aprendizaje y la memoria se ha convertido en una tarea de interés para muchos investigadores. Artículos recientes han podido comprobar es que el ejercicio es una clara herramienta para mejorar capacidades cognitivas de personas y animales gracias a que favorece la liberación de sustancias tales como neurotransmisores y factores neurotróficos. Uno de los factores más importantes es el factor neurotrófico derivado del cerebro (BDNF), que promueve la generación de cambios a nivel neuronal necesarios para la potenciación a largo plazo (fortalecimiento de memorias). Se realizó una búsqueda en las bases de datos de EBSCOhost -en las bases de Academic Search Complete, ERIC, MEDLINE, PsycARTICLES y SPORTDiscus-, Google Scholar, Pubmed y ScienceDirect utilizando una serie de palabras con sus respectivos criterios de inclusión y exclusión. En este trabajo se explican los procesos asociados con la potenciación a largo plazo, abarcando temas como neuroplasticidad, la unión del BDNF con su receptor (receptores de tirosina quinasa B), y además el mecanismo por medio del cual la liberación de la mioquina irisina, como una consecuencia del ejercicio, promueve el aumento de las concentraciones de BDNF en sangre. Basándose en numerosa literatura se describe la relación que existe entre el ejercicio y la generación de cambios neuroplásticos estimulados por proteínas como el BDNF y la consecuente mejoría en la memoria.

Timing matters: The interplay of the retrieval frequency and temporal distance between retrieving a prior list and encoding a new list in vocabulary retention

The act of retrieval yields benefits for memory. However, according to the reconsolidation account, reactivation could render a memory amenable to modifications. The present study investigated how the retrieval frequency of a previously learned vocabulary list and the temporal distance of a subsequently encoded list affected retention of the prior list. Recruited from six intact sessions of a college intensive English course, participants learned two unrelated lists of novel words and took cued-recall tests. The results revealed an interaction between the retrieval of list 1 (single vs. repeated) and the encoding of list 2 (close vs. far vs. no). Noteworthy, the repeated-retrievals groups outperformed single-retrieval groups only when list 2 encoding was spaced far apart (i.e., 3-day interval). The memory impairment effect emerged in the presence of list 2 whereas the memory strengthening effect occurred in the absence of list 2. These results suggest that the interplay between repeated retrievals and an extended temporal distance functions in a way that may attenuate memory’s susceptibility to new learning rather than abolish it. Situated in the naturalistic classroom setting, these findings have pedagogical significance for instructors to schedule testing and learning sessions to help learners optimize vocabulary retention.

Activity-Dependent Plasticity at Associative Memory Cells in the Prefrontal Cortex

In addition to structural and functional alternations of neurons during their recruitment to be associative memory cells, these associative memory cells undergo the functional plasticity in response to their activity, called as recruitment-relevant plasticity and activity-dependent plasticity, respectively (Associative Memory Cells: Basic Units of Memory Trace by Jin-Hui Wang 2019). Here, we report the features of activity-dependent plasticity at associative memory cells studied by two-photon cell imaging. After the learning of triple associated signals (pair-stimulations by odor, whisker tactile and tail warming-up), secondary associative memory cells in response to these signals are recruited in the prefrontal cortex. The portion of functional associative memory cells is upregulated by intensive activity in one of three synaptic inputs or their combinations. When whisker, odor or tail stimulus is given intensively, the activity levels of these associative memory cells show low-to-high or high-to-low in response to original cues, especially activity-dependent depression in response to homosynaptic signal and activity-dependent potentiation in response to heterosynaptic signal. When whisker, odor and tail stimulations are given simultaneously, these associative memory cells express activity-dependent potentiation in response to all these input signals. The upregulated activities of norepinephrine and serotonin in the central nervous system strengthen the recruitment, the functional strength and the activity-dependent plasticity of associative memory cell in response to homosynaptic and heterosynaptic signals. As activity-dependent plasticity at associative memory cells occurs immediately after their activation, our results may be due to a possibility that the new synapses formed on associative memory cells during associative learning can be upregulated and downregulated between active state and inactive state, in which their intensive activities and monoamine neurotransmitters are critical modulators. The results can explain activity-related memory strengthening and the role of the arousal system through norepinephrine and serotonin in memory.

Revisiting metaplasticity: The roles of calcineurin and histone deacetylation in unlearning odor preference memory in rat pups.

Previous work has shown that 24 h duration odor preference learning, induced by one-trial training, generates a down-regulation of the GluN1 receptor in anterior piriform cortex at 3 h, and results in metaplastic unlearning if a second training trial is given at 3 h. The GluN1 receptor upregulates at 24 h so 24 h spaced training is highly effective in extending memory duration. The present study replicates the piriform cortex unlearning result in the olfactory bulb circuit and further studies the relationship between the initial training strength and its associated metaplastic effect. Intrabulbar infusions that block calcineurin or inhibit histone deacetylation normally produce extended days-long memory. If given during training, they are not associated with GluN1 downregulation at 3 h and do not recruit an unlearning process at that time. The two memory strengthening protocols do not appear to interact, but are also not synergistic. These outcomes argue that it is critical to understand the metaplastic effects of training in order to optimize training protocols in the service of either memory strengthening or of memory weakening.

Multiple-object Tracking as a Tool for Parametrically Modulating Memory Reactivation.

Converging evidence supports the "nonmonotonic plasticity" hypothesis, which states that although complete retrieval may strengthen memories, partial retrieval weakens them. Yet, the classic experimental paradigms used to study effects of partial retrieval are not ideally suited to doing so, because they lack the parametric control needed to ensure that the memory is activated to the appropriate degree (i.e., that there is some retrieval but not enough to cause memory strengthening). Here, we present a novel procedure designed to accommodate this need. After participants learned a list of word-scene associates, they completed a cued mental visualization task that was combined with a multiple-object tracking (MOT) procedure, which we selected for its ability to interfere with mental visualization in a parametrically adjustable way (by varying the number of MOT targets). We also used fMRI data to successfully train an "associative recall" classifier for use in this task: This classifier revealed greater memory reactivation during trials in which associative memories were cued while participants tracked one, rather than five, MOT targets. However, the classifier was insensitive to task difficulty when recall was not taking place, suggesting that it had indeed tracked memory reactivation rather than task difficulty per se. Consistent with the classifier findings, participants' introspective ratings of visualization vividness were modulated by MOT task difficulty. In addition, we observed reduced classifier output and slowing of responses in a postreactivation memory test, consistent with the hypothesis that partial reactivation, induced by MOT, weakened memory. These results serve as a "proof of concept" that MOT can be used to parametrically modulate memory retrieval-a property that may prove useful in future investigation of partial retrieval effects, for example, in closed-loop experiments.

0234 LOSING MEMORIES WITH TARGETED MEMORY REACTIVATION

Targeted memory reactivation during sleep is a powerful tool to influence the mind. Current literature demonstrates memory strengthening following targeted memory reactivation (TMR) using sounds or odors (see Oudiette & Paller, 2013 for review). Here we investigate whether TMR-forget can successfully induce episodic memory loss. Eighteen participants were administered two learning tasks before sleeping. First, participants were trained on a forget cue where they viewed 46 words, half of which were followed by the cue. Then participants learned 28 novel object-location pairs that were paired with their associated sounds. From these objects, five were randomly chosen for reactivation and five others for controls. That night, during the first period of SWS, we reactivated the five objects with the forget tone 20 times each. Seven days later, we tested participants’ memories of the objects, their locations, and the words using free-recall and recognition. Seven days later, participants recalled fewer reactivated than control objects (t(1,17)=3.682 p = .002, Cohen’s d = 1.23). Reactivated objects that were not recalled were also less likely to be correctly located than those that were recalled (t(1,15) = -2.132 p = .05, Cohen’s d = .764) and had lower confidence ratings (t(1,15) = -5.558 p >.001, Cohen’s d = 1.983). No stage of sleep (N1, N2, N3, or REM) correlated with later forgetting (r’s ≥ -.177, p’s ≥ .383). N1, N2, and REM did not correlate with control retention (r’s ≥ .072, p’s ≥ .494), however we found a trending correlation for N3 (r = .465, p = .07). We demonstrate that TMR-forget can successfully induce episodic memory loss for objects one week later. Participants are less likely to recall the reactivated objects as well as less likely to correctly spatially locate those they successfully forgot. It will be important for future studies to determine whether TMR-forget can induce loss of emotional memories, which will lead the way for novel therapeutic interventions for disorders such as PTSD or specific phobias. Not applicable.

Selectivity in Postencoding Connectivity with High-Level Visual Cortex Is Associated with Reward-Motivated Memory

Reward motivation has been demonstrated to enhance declarative memory by facilitating systems-level consolidation. Although high-reward information is often intermixed with lower reward information during an experience, memory for high value information is prioritized. How is this selectivity achieved? One possibility is that postencoding consolidation processes bias memory strengthening to those representations associated with higher reward. To test this hypothesis, we investigated the influence of differential reward motivation on the selectivity of postencoding markers of systems-level memory consolidation. Human participants encoded intermixed, trial-unique memoranda that were associated with either high or low-value during fMRI acquisition. Encoding was interleaved with periods of rest, allowing us to investigate experience-dependent changes in connectivity as they related to later memory. Behaviorally, we found that reward motivation enhanced 24 h associative memory. Analysis of patterns of postencoding connectivity showed that, even though learning trials were intermixed, there was significantly greater connectivity with regions of high-level, category-selective visual cortex associated with high-reward trials. Specifically, increased connectivity of category-selective visual cortex with both the VTA and the anterior hippocampus predicted associative memory for high- but not low-reward memories. Critically, these results were independent of encoding-related connectivity and univariate activity measures. Thus, these findings support a model by which the selective stabilization of memories for salient events is supported by postencoding interactions with sensory cortex associated with reward. <b>SIGNIFICANCE STATEMENT</b> Reward motivation is thought to promote memory by supporting memory consolidation. Yet, little is known as to how brain selects relevant information for subsequent consolidation based on reward. We show that experience-dependent changes in connectivity of both the anterior hippocampus and the VTA with high-level visual cortex selectively predicts memory for high-reward memoranda at a 24 h delay. These findings provide evidence for a novel mechanism guiding the consolidation of memories for valuable events, namely, postencoding interactions between neural systems supporting mesolimbic dopamine activation, episodic memory, and perception.

Selectivity in Postencoding Connectivity with High-Level Visual Cortex Is Associated with Reward-Motivated Memory.

Reward motivation is thought to promote memory by supporting memory consolidation. Yet, little is known as to how brain selects relevant information for subsequent consolidation based on reward. We show that experience-dependent changes in connectivity of both the anterior hippocampus and the VTA with high-level visual cortex selectively predicts memory for high-reward memoranda at a 24 h delay. These findings provide evidence for a novel mechanism guiding the consolidation of memories for valuable events, namely, postencoding interactions between neural systems supporting mesolimbic dopamine activation, episodic memory, and perception.

Direct dorsal hippocampal-prelimbic cortex connections strengthen fear memories.

The ability to regulate the consolidation and strengthening of memories for threatening experiences is critical for mental health, and its dysregulation may lead to psychopathologies. Re-exposure to the context in which the threat was experienced can either increase or decrease fear response through distinct processes known, respectively, as reconsolidation or extinction. Using a context retrieval-dependent memory enhancement paradigm in rats, we report that memory strengthens through the activation of direct projections from the dorsal hippocampus (dHC) to the prelimbic (PL) cortex and of critical PL molecular mechanisms, which are not required for extinction. Furthermore, while a sustained PL BDNF expression is required for memory consolidation, retrieval engages PL BDNF to regulate the excitatory and inhibitory synaptic proteins neuroligin 1 and neuroligin 2, which promote memory strengthening while inhibiting extinction. Thus, context retrieval-mediated fear memory enhancement results from a concerted action of mechanisms that strengthen memory through reconsolidation while suppressing extinction.

Phosphoproteomic Analysis Reveals a Novel Mechanism of CaMKII Regulation Inversely Induced by Cocaine Memory Extinction versus Reconsolidation

Successful addiction treatment depends on maintaining long-term abstinence, making relapse prevention an essential therapeutic goal. However, exposure to environmental cues associated with drug use often thwarts abstinence efforts by triggering drug using memories that drive craving and relapse. We sought to develop a dual approach for weakening cocaine memories through phosphoproteomic identification of targets regulated in opposite directions by memory extinction compared with reconsolidation in male Sprague-Dawley rats that had been trained to self-administer cocaine paired with an audiovisual cue. We discovered a novel, inversely regulated, memory-dependent phosphorylation event on calcium-calmodulin-dependent kinase II α (CaMKIIα) at serine (S)331. Correspondingly, extinction-associated S331 phosphorylation inhibited CaMKIIα activity. Intra-basolateral amygdala inhibition of CaMKII promoted memory extinction and disrupted reconsolidation, leading to a reduction in subsequent cue-induced reinstatement. CaMKII inhibition had no effect if the memory was neither retrieved nor extinguished. Therefore, inhibition of CaMKII represents a novel mechanism for memory-based addiction treatment that leverages both extinction enhancement and reconsolidation disruption to reduce relapse-like behavior. Preventing relapse to drug use is an important goal for the successful treatment of addictive disorders. Relapse-prevention therapies attempt to interfere with drug-associated memories, but are often hindered by unintentional memory strengthening. In this study, we identify phosphorylation events that are bidirectionally regulated by the reconsolidation versus extinction of a cocaine-associated memory, including a novel site on CaMKIIα. Additionally, using a rodent model of addiction, we show that CaMKII inhibition in the amygdala can reduce relapse-like behavior. Together, our data supports the existence of mechanisms that can be used to enhance current strategies for addiction treatment.

Sleep Strengthens but does Not Reorganize Memory Traces in a Verbal Creativity Task.

Sleep after learning promotes the quantitative strengthening of new memories. Less is known about the impact of sleep on the qualitative reorganization of memory content. This study tested the hypothesis that sleep facilitates both memory strengthening and reorganization as indexed by a verbal creativity task. Sixty healthy university students (30 female, 30 male, 20-30 years) were investigated in a randomized, controlled parallel-group study with three experimental groups (sleep, sleep deprivation, daytime wakefulness). At baseline, 60 items of the Compound Remote Associate (CRA) task were presented. At retest after the experimental conditions, the same items were presented again together with 20 new control items to disentangle off-line incubation from online performance effects. Sleep significantly strengthened formerly encoded memories in comparison to both wake conditions (improvement in speed of correctly resolved items). Offline reorganization was not enhanced following sleep, but was enhanced following sleep-deprivation in comparison to sleep and daytime wakefulness (solution time of previously incubated, newly solved items). Online performance did not differ between the groups (solution time of new control items). The results support the notion that sleep promotes the strengthening, but not the reorganization, of newly encoded memory traces in a verbal creativity task. Future studies are needed to further determine the impact of sleep on different types of memory reorganization, such as associative thinking, creativity and emotional memory processing, and potential clinical translations, such as the augmentation of psychotherapy through sleep interventions.