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Task switching is a behavioral phenomenon that serves as a tool for assessment of individual cognitive abilities that becomes especially essential in our multitasking milieu. Factors of task-switching include cognitive load and cognitive effort, mostly derived from task difficulty, as well as age and practice. The analysis of brain activity on the level of single neurons shows that the activations that contribute to task performance and switching differ with respect to the protocol of learning the alternated tasks. We argue that task switching is affected by the history of learning and in turn it changes the structure of individual experience. On this basis we outline perspectives of task switching studies in the fundamental field of long-term memory and applied field of education and therapy.

Using pre-trained topic information to assist in training neural networks can effectively support the completion of the rating prediction task. However, existing neural-topic methods consider only the use of topic information corresponding to current users and items without neighbors, whereas existing memory-based neighborhood approaches are inappropriate for the direct modeling of neighbors with topics. To address the limitations, we argue that memory networks have the ability to organize neighbors with corresponding topics well and can provide a general solution to this problem. To confirm our hypothesis, we propose two approaches. One is an augmented memory network to couple with and enhance existing neural-topic models. The other is a symmetric memory network activated by a memory reorganization mechanism, which is a compact and generalized method for rating prediction. The experimental results demonstrate the effectiveness of the memory reorganization mechanism and show that the two proposed methods have advantages over existing state-of-the-art topic modeling approaches.

Task switching is a behavioral phenomenon that serves as a tool for assessment of individual cognitive abilities that becomes especially essential in our multitasking milieu. Factors of task-switching include cognitive load and cognitive effort, mostly derived from task difficulty, as well as age and practice. The analysis of brain activity on the level of single neurons shows that the activations that contribute to task performance and switching differ with respect to the protocol of learning the alternated tasks. We argue that task switching is affected by the history of learning and in turn it changes the structure of individual experience. On this basis we outline perspectives of task switching studies in the fundamental field of long-term memory and applied field of education and therapy. [ABSTRACT FROM AUTHOR]

Highlights • Adaptive recruitments of neurons within memory circuit were observed in TLE patients. • Extra-temporal recruitment was identified during the pre-operative period. • Shifted recruitment to ipsilateral temporal lobe was noted after the surgery. Abstract This study was aimed to longitudinally assess memory function and whole-brain memory circuit reorganization in patients with temporal lobe epilepsy (TLE) by comparing activation potentials before versus after anterior temporal lobe (ATL) resection. Nineteen patients with medically-intractable TLE (10 left TLE, 9 right TLE) and 15 healthy controls were enrolled. Group analyses were conducted pre- and post-ATL of a novelty complex scene-encoding paradigm comparing areas of blood oxygen-level-dependent (BOLD) signal activations on functional magnetic resonance imaging (fMRI). None of the pre-operative patient characteristics we studied predicted the extent of pre- to post-operative memory loss. On fMRI, extra-temporal activations were detected pre-operatively in both LTLE and RTLE, particularly in the frontal lobe. Greater activations also were noted in the contralateral hippocampus and parahippocampus in both groups. Performing within-subject comparisons, post-op relative to pre-op, pronounced ipsilateral activations were identified in the left parahippocampal gyrus in LTLE, versus the right middle temporal gyrus in RTLE patients. Memory function was impaired pre-operatively but declined after ATL resection in both RTLE and LTLE patients. Post-operative fMRI results indicate possible functional adaptations to ATL loss, primarily occurring within the left parahippocampal gyrus versus right middle temporal gyrus in LTLE versus RTLE patients, respectively. [ABSTRACT FROM AUTHOR]

Memory reconsolidation processes and protein kinase Mzeta (PKMzeta) activity in memory maintenance and reorganization are poorly understood. Therefore, we examined memory reconsolidation and PKMzeta activity during the maintenance and reorganization of a conditioned food aversion memory among snails. These processes were specifically evaluated after administration of a serotonin receptor antagonist (methiothepin), NMDA glutamate receptor antagonist (MK-801), protein synthesis inhibitor (cycloheximide; CYH), or PKMzeta inhibitor (zeta inhibitory peptide; ZIP) either 2 or 10 days after aversion training. Two days post-training, injections of MK-801 or CYH, combined with a conditioned stimulus reminder, caused amnesia development, and a second training 11 days after this induction did not lead to long-term memory formation. Interestingly, MK-801 or CYH injections and the reminder 10 days after training did not affect memory retrieval. Methiothepin and the reminder, or ZIP without the reminder, at 2 and 10 days after training led to memory impairment, while a second training 11 days after amnesia induction resulted in memory formation. These results suggest that the maintenance of a conditioned food aversion involves two different components with variable dynamics. One component could be characterized by memory strengthening over time and involve N -methyl- D -aspartate receptors and protein synthesis reconsolidation at early, but not late, training stages. The other memory component could involve serotonin-dependent reconsolidation and Mzeta-like kinase activity at both early and late stages after learning. Deficiencies within these two components led to various forms of memory impairment, which differed in terms of the formation of a conditioned food aversion during the second training. [ABSTRACT FROM AUTHOR]

1.25 mg/kg) given without a reminder two days after training were ineffective, while ZIP (2.5 mg/kg) evoked transient memory impairment one day after injection with spontaneous recovery on day 10. Injections of ZIP (5 mg/kg) without a reminder led to memory impairment and the development of stable amnesia. On repeat training of animals 11 days after induction of amnesia induced by ZIP (5 mg/kg), the number of combined food and reinforcement stimuli required to form the memory was similar to that in initial training. ZIP (5 and 10 mg/kg) combined with a reminder induced amnesia, though repeat training at 11 days led to dose-dependent increases in the rate of formation of memory than on initial training. It is suggested that in snails trained to conditioned food aversion, inhibition of a PKMzeta-like enzyme without a reminder induced 'fading of the memory trace,' while repeat training formed a new memory. PKMzeta is evidently not directly involved in the process of memory reconsolidation, though reminding prevented the amnestic effect of ZIP. [ABSTRACT FROM AUTHOR]

Memory is a reference formed from a past experience that is used to respond to present situations. However, the world is dynamic and situations change, so it is important to update the memory with new information each time it is reactivated in order to adjust the response in the future. Recent researches indicate that memory may undergo a dynamic process that could work as an updating mechanism. This process which is called reconsolidation involves destabilization of the memory after it is reactivated, followed by restabilization. Recently, it has been demonstrated that the initial destabilization process of reconsolidation requires protein degradation. Using protein degradation inhibition as a method to block reconsolidation, recent researches suggest that reconsolidation, especially the protein degradation-dependent destabilization process is necessary for memory reorganization.

The memory reconsolidation hypothesis suggests that a memory trace becomes labile after retrieval and needs to be reconsolidated before it can be stabilized. However, it is unclear from earlier studies whether the same synapses involved in encoding the memory trace are those that are destabilized and restabilized after the synaptic reactivation that accompanies memory retrieval, or whether new and different synapses are recruited. To address this issue, we studied a simple nonassociative form of memory, long-term sensitization of the gill- and siphon-withdrawal reflex in Aplysia, and its cellular analog, long-term facilitation at the sensory-to-motor neuron synapse. We found that after memory retrieval, behavioral long-term sensitization in Aplysia becomes labile via ubiquitin/proteasome-dependent protein degradation and is reconsolidated by means of de novo protein synthesis. In parallel, we found that on the cellular level, long-term facilitation at the sensory-to-motor neuron synapse that mediates long-term sensitization is also destabilized by protein degradation and is restabilized by protein synthesis after synaptic reactivation, a procedure that parallels memory retrieval or retraining evident on the behavioral level. These results provide direct evidence that the same synapses that store the long-term memory trace encoded by changes in the strength of synaptic connections critical for sensitization are disrupted and reconstructed after signal retrieval. [ABSTRACT FROM AUTHOR]

An accumulating body of evidence shows that reactivated long-term memory undergoes a dynamic process called reconsolidation, in which de novo protein synthesis is required to maintain the memory. These findings open up a new dimension in the field of memory research. However, few studies have shown how once-consolidated memory becomes labile. The authors' recent findings have demonstrated that preexisting long-term memory becomes unstable via the ubiquitin/ proteasome-dependent protein degradation pathway and that this labile state is required for the reorganization of fear memory. Here, the authors review this finding and focus on the labile state that is critical for the reorganization of memory triggered after memory retrieval. [ABSTRACT FROM AUTHOR]

Abstract: Growing evidence indicates a role for sleep in off-line memory processing, specifically in post-training consolidation. In humans, sleep has been shown to trigger overnight learning on a motor-sequence memory task, while equivalent waking periods produce no such improvement. But while the behavioral characteristics of sleep-dependent motor learning become increasingly well characterized, the underlying neural basis remains unknown. Here we present functional magnetic resonance imaging data demonstrating a change in the representation of a motor memory after a night of sleep. Subjects trained on a motor-skill memory and 12 hours later, after either sleep or wake, were retested during functional magnetic resonance imaging. Following sleep relative to wake, regions of increased activation were expressed in the right primary motor cortex, medial prefrontal lobe, hippocampus and left cerebellum; changes that can support faster motor output and more precise mapping of key-press movements. In contrast, signal decreases were identified in parietal cortices, the left insular cortex, temporal pole and fronto-polar region, reflecting a reduced need for conscious spatial monitoring and a decreased emotional task burden. This evidence of an overnight, systems-level change in the representation of a motor memory holds important implications for acquiring real-life skills and in clinical rehabilitation following brain trauma, such as stroke. [Copyright &y& Elsevier]

Several studies have shown that memory circuits can be reorganised as a function of age. Brain magnetic activity evoked by a memory task was recorded in 19 healthy elderly subjects divided into two groups, a young-elder group (mean age of 62) and senior-elder group (mean age of 76). The young-elder group showed greater activity over the left medial temporal lobe in the late latency windows (between 400 and 800 ms) than the senior-elder group. The senior-elder group showed an initial increased activity (between 150 and 400 ms) over the complex of motor areas, followed by an increased activity in the left temporo-parietal cortex at the late latency window. These results revealed a reorganization of brain networks supporting memory in the eldest subjects. Furthermore, these circuits are reorganised in a time-dependent manner, meaning the rehearsal articulatory process active in the early time window followed by a phonological storage and recognition process in the late latency window. [Copyright &y& Elsevier]

Memories are thought to become more gist-like over time. Multiple related memories might form generalized memory representations, losing specific details but enhancing or retaining gist. The time course within which gist memory emerges, however, is the subject of less consensus. To address this question, we focused our design on four kinds of gist: inferential gist (relations extracted across non-contiguous events), statistical learning (regularities extracted from a series), summary gist (a theme abstracted from a temporally contiguous series of items), and category gist (characterization of a stimulus at a higher level in the semantic hierarchy). Seventy participants completed memory encoding tasks addressing these types of gist and corresponding retrieval tasks the same evening, the morning after, and one week later, as well as an MRI at a later time point. We found little evidence that gist slowly emerges over time or that gist traces are more resistant to forgetting than detail traces. Instead, we found that initial gist memory shortly after encoding was either retained over time or decayed. Inferential gist and statistical learning were retained over a week, whereas memory for category and summary gist decayed. We discuss several interpretations for differences between these two subtypes of gist. Individual differences in REM or slow-wave sleep and hippocampal volumes did not predict changes in memory for these four kinds of gist in a healthy young adult population. [ABSTRACT FROM AUTHOR]

Temporal lobe epilepsy is associated with impairment in episodic memory. A substantial subgroup, however, is able to maintain adequate memory despite temporal lobe pathology. Missing from prior work in cognitive reorganization is a direct comparison of temporal lobe epilepsy patients with intact status with those who are memory impaired. Little is known about the regional activations, functional connectivities and/or network reconfigurations that implement changes in primary computations or support functions that drive adaptive plasticity and compensated memory. We utilized task functional MRI on 54 unilateral temporal lobe epilepsy patients and 24 matched healthy controls during the performance of a paired-associate memory task to address three questions: (i) which regions implement paired-associate memory in temporal lobe epilepsy, and do they vary as a function of good versus poor performance, (ii) is there unique functional connectivity present during memory encoding that accounts for intact status by preservation of primary memory computations or the supportive computations that allow for intact memory responses and (iii) what features during memory encoding are most distinctive: is it the magnitude and location of regional activations, or the presence of enhanced functional connections to key structures such as the hippocampus? The study revealed non-dominant hemisphere regions (right posterior temporal regions) involving both increased regional activity and increased modulatory communication with the hippocampi as most important to intact memory in left temporal lobe epilepsy compared to impaired status. The profile involved areas that are neither contralateral homologues to left hemisphere memory areas, nor regions traditionally considered computationally primary for episodic memory. None of these areas of increased activation or functional connectivity were associated with advantaged memory in healthy controls. Our emphasis on different performance levels yielded insight into two forms of cognitive reorganization: computational primacy, where left temporal lobe epilepsy showed little change relative to healthy controls, and computational support where intact left temporal lobe epilepsy patients showed adaptive abnormalities. The analyses isolated the unique regional activations and mediating functional connectivity that implements truly compensatory reorganization in left temporal lobe epilepsy. The results provided a new perspective on memory deficits by making clear that they arise not just from the knockout of a functional hub, but from the failure to instantiate a complex set of reorganization responses. Such responses provided the computational support to ensure successful memory. We demonstrated that by keeping track of performance levels, we can increase understanding of adaptive brain responses and neuroplasticity in epilepsy., (© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.)

Memory is a reference formed from a past experience that is used to respond to present situations. However, the world is dynamic and situations change, so it is important to update the memory with new information each time it is reactivated in order to adjust the response in the future. Recent researches indicate that memory may undergo a dynamic process that could work as an updating mechanism. This process which is called reconsolidation involves destabilization of the memory after it is reactivated, followed by restabilization. Recently, it has been demonstrated that the initial destabilization process of reconsolidation requires protein degradation. Using protein degradation inhibition as a method to block reconsolidation, recent researches suggest that reconsolidation, especially the protein degradation-dependent destabilization process is necessary for memory reorganization.