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Neurobiological systems regulating memory consolidation. Experiences activate timedependent cellular storage processes in various brain regions involved in the forms of memory represented. The experiences also initiate the release of the stress hormones from the adrenal medulla and adrenal cortex and activate the release of norepinephrine in the basolateral amygdala, an effect critical for enabling modulation of consolidation. The amygdala modulates memory consolidation by influencing neuroplasticity in other brain regions.
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The memory consolidation hypothesis proposed 100 years ago by Müller and Pilzecker continues to guide memory research. The
hypothesis that new memories consolidate slowly over time has stimulated studies revealing the hormonal and neural influences
regulating memory consolidation, as well as molecular and cellular mechanisms. This review examines t...
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... on vagal affer- ents projecting to the nucleus of the solitary tract in the brainstem. Noradrenergic projec- tions from this region influence neuronal ac- tivity in other brain regions, including the amygdala (20). Glucocorticoids released from the adrenal cortex readily enter the brain and activate intracellular glucocorticoid re- ceptors ( Fig. 2). Activation of the amygdala, a brain region important for emotional arous- al, is critical for mediating the influences of epinephrine and glucocorticoids, because amygdala lesions block the effects of these modulators on consolidation. Most important, activation of -adrenergic receptors in the amygdala is essential. Infusions of ...
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Citations
... To isolate the effects of oxytocin on memory consolidation, we used a post-study design (i.e., oxytocin administrated after memory encoding) based on memory consolidation studies in both animals and humans 10,11 . This is the standard paradigm to evaluate and isolate the effects of certain experimental manipulations (e.g., physical exercise 12 , caffeine intake 13 , brain stimulation 14 , and emotional arousal 15,16 ) on memory consolidation. ...
Oxytocin plays a critical role in modulating social cognition and enhancing human memory for faces. However, it remains unclear which stage of memory oxytocin affects to enhance face memory. Our study explored oxytocin’s potential to selectively enhance the consolidation of social memories, specifically human faces, and whether this effect varies between genders. In two preregistered, randomized, double-blind, placebo-controlled trials with heterosexual participants (total N=294, comprising 149 males and 145 females), we explored how oxytocin affects memory consolidation. We administered oxytocin immediately after encoding (i.e., Study1) and 30 minutes before retrieval in a parallel study (i.e., Study2). This design allowed us to confirm that oxytocin’s effects were indeed due to consolidation rather than retrieval. We found that administering oxytocin post-encoding, but not before-retrieval, significantly improved female participants’ ability to recognize male faces 24 hours later, with no similar enhancement observed in males recognizing opposite-gender faces. Together with our analyses of social placebo effects and approachability rating during encoding, we concluded that oxytocin enhanced consolidation of long-term social memories in humans. Our results not only advance the understanding of the neurobiological mechanisms underlying social memory consolidation but also highlight oxytocin as a pharmacological tool for selectively enhancing human memory consolidation.
Highlights
Oxytocin selectively enhances memory consolidation of human faces, with gender-specific effects.
In females, oxytocin after encoding improves recognition of male faces after 24 hours.
Oxytocin-induced enhancement of social memory is due to enhanced consolidation, not retrieval or encoding.
Oxytocin shows potential for selectively modulating memory consolidation in humans.
... The process of memory encoding involves various neural mechanisms such as neurochemical changes and synaptic plasticity [13,14]. Then, the process of consolidation and long-term maintenance of this memory involves a complex set of neural and molecular mechanisms that enable information to be retained over extended periods of time [15]. In particular during sleep and resting state of the brain, generally characterized by slow and asynchronous irregular dynamics [16], short phases of partially synchronous activation or series of sequence activation-which can be linked to spontaneous recalls or replays of learned information-occur promoting memory consolidation [17][18][19]. ...
In the last three decades the field of brain connectivity has uncovered that cortical regions, interconnected via white-matter fibers, form a modular and hierarchical network. This type of organization, which has also been recognised at the microscopic level in the form of interconnected neural assemblies, is typically believed to support the coexistence of segregation (specialization) and integration (binding) of information. A prominent remaining question is to understand how the brain could possibly become such a complex network. Here, we give a first step into answering this question and propose that adaptation to various inputs could be the key driving mechanism for the formation of structural assemblies at different scales. To illustrate that, we develop a model of (QIF) spiking neurons, subjected to stimuli targetting distributed populations. The model follows several biologically plausible constraints: (i) it contains both excitatory and inhibitory neurons with two classes of plasticity: Hebbian and anti-Hebbian STDP, (ii) dynamics are not frozen after the entrainment is finished but the network is allowed to continue firing spontaneously, and (iii) plasticity remains always active, also after the learning phase. We find that only the combination of Hebbian and anti-Hebbian inhibitory plasticity allows the formation of stable modular organization in the network. Besides, given that the model continues ``alive'' after the learning, the network settles into an asynchronous irregular firing state displaying spontaneous memory recalls which, as we show, turn crucial for the long-term consolidation of the learned memories.
... Originally, a consolidated memory was seen as permanently fixed and insensitive to disruption by the kind of amnesic interventions that are effective shortly after initial acquisition, i.e., before consolidation has taken place (McGaugh, 2000). However, in the late 1960s, soon after the formalization of the memory consolidation theory (McGaugh, 1966), a landmark study conducted by Misanin, Miller, and Lewis, (1968;also see Schneider & Sherman, 1968) documented in non-human animals that memories could be rendered vulnerable to amnesic interventions 24 h after training occurred, long after consolidation should have been completed. ...
... Around the same time that influential psychological models for memory were being developed (e.g., Atkinson & Estes, 1963;Bush & Mosteller, 1951;Miller, 1955), the biological mechanisms subserving how new information is encoded in the brain were also receiving intensive attention (Hebb, 1949). In particular, memory consolidation theory (for classical reviews about the literature on time-dependent modulation of memory, see McGaugh, 1966McGaugh, , 2000 and long-term potentiation (LTP; Bliss & Lomo, 1973) were proposed as key neurobiological processes and substrates for memory storage. These phenomena and their connections to behaviour reflecting memory have been reviewed extensively (e.g., Lynch, 2004;Malenka & Nicoll, 1999;McGaugh, 2000), and a detailed overview of this evidence is beyond the scope of the current review. ...
... In particular, memory consolidation theory (for classical reviews about the literature on time-dependent modulation of memory, see McGaugh, 1966McGaugh, , 2000 and long-term potentiation (LTP; Bliss & Lomo, 1973) were proposed as key neurobiological processes and substrates for memory storage. These phenomena and their connections to behaviour reflecting memory have been reviewed extensively (e.g., Lynch, 2004;Malenka & Nicoll, 1999;McGaugh, 2000), and a detailed overview of this evidence is beyond the scope of the current review. ...
A canonical view in the neuroscience of learning and memory literature is that failures in memory expression reflect storage failures, and hence amnesic manipulations following training or following memory reactivation can permanently erase memory traces. In this review, we analyse extant literatures from the learning and memory domains suggesting that most if not all of these memory deficits can be restored with the appropriate retrieval cues. We content that all manipulations conducted immediately after training or following memory reactivation result in new learning, which is highly dependent on retrieval cues for memory expression. Thus, although acquisition and storage mechanisms are important, memory retrieval is a critical component of memory performance, with numerous findings from behavioural and neurobiological studies all converging on this general notion. These conclusions invite a rethinking of the learning and memory literatures and provide new avenues for research.
... Decades of extinction studies that never eliminated the target learning led researchers to the conclusion that once an emotional learning has become a long-term memory through the process of consolidation (reviewed by McGaugh, 2000), it is "indelible" for the lifetime of the individual (LeDoux et al., 1989). There appeared to exist no form of neuroplasticity capable of unlocking the neural encoding of consolidated emotional learnings. ...
A person’s “memory” is the stored form of all types of acquired personal knowledge, including both knowledge of personal experiences (episodic memory) and knowledge of patterns perceived in the world (semantic memory), such as the knowledge that staying safe around one’s rage-prone, alcoholic parent urgently requires never expressing any views or feelings of one’s own. This article explores the possibility of (a) understanding most, if not all, psychotherapeutic action as a reconfiguration of knowledge held in memory and (b) identifying each of the distinct, fundamentally different endogenous mechanisms, or types of processes, that can modify memory therapeutically. In this way, a potential means of unifying psychotherapy emerges, enabling us to identify how any particular therapeutic process influences symptom production through its memory modification effects. Memory neuroscience has identified mechanisms of memory modification sufficiently for the proposed explorations to be pursued fruitfully at this point. The resulting unification scheme consists of two qualitatively different, main modes of memory modification, each with submodes. This scheme can account for the full range of therapeutic outcomes, from partial, unstable, relapse-prone symptom reduction to transformational change, defined here as the enduring cessation of a symptom and its underlying theme of emotional distress. Case vignettes illustrate the fundamental modes and some submodes of therapeutic memory modification. Viewed through this unification framework, diverse therapy systems no longer seem to belong to different worlds. Rather, their distinctive techniques and methodologies become a rich array of options for tailoring memory modification and therapeutic change uniquely for each person.
... Memory in rodents can be tested by a step-down model of inhibitory avoidance tasks [16]. The results obtained in the present study indicated that post-training or pre-test intra-CA1 administration of WIN55,212-2 impaired memory retrieval on the test day. ...
In the present study, the possible role of �1-adrenergic receptors of the dorsal hippocampus on
WIN55,212-2-induced amnesia in male Wistar rats has been evaluated. As a model of learning, a
step-down passive avoidance task was used. Results indicated that post-training or pre-test intra-
CA1 administration of WIN55,212-2 (0.25 and 0.5�g/rat) reduced the step-down latency, showing
an amnestic response. Amnesia produced by post-training WIN55,212-2 (0.5�g/rat) was reversed by
pre-test administration of the same drug dose. Interestingly, pre-test intra-CA1 administration of �1-
noradrenergic agonists, phenylephrine alone or with an ineffective dose of WIN55,212-2 (0.25�g/rat)
reversed post-training WIN55,212-2 (0.5�g/rat)-induced retrieval impairment. On the other hand,
pre-test intra-CA1 microinjection of an �1-adrenergic antagonist, prazosin (0.5�g/rat), 2 min before
administration of WIN55,212-2 (0.5�g/rat) inhibited the pre-test WIN55,212-2 response. It may
be concluded that �1-adrenergic receptors of the dorsal hippocampal CA1 regions play an important
role in WIN55,212-2-induced amnesia and restoration of memory by pre-test WIN55,212-2
administration.
... Exerciseinduced shifts in participant's bias would be expected to influence performance on tests of recognition memory. Neurophysiological models of long-term memory propose that item familiarity is altered by emotional arousal and the biological stress response when exercise follows encoding, which is characterized by a cascade of neurohormonal changes (Loprinzi et al., 2019a(Loprinzi et al., ,b, 2020a(Loprinzi et al., ,b, 2021McGaugh, 2000McGaugh, , 2004McGaugh, , 2018. The release of adrenal stress hormones results in widespread changes throughout the peripheral and central nervous system. ...
Research findings reveal a relationship between acute bouts of exercise and procedural/declarative memory. Prior systematic reviews report small/moderate effects of acute exercise on episodic long-term declarative memory. A somewhat overlooked issue is the influence of exercise on specific types of episodic memory processing. The primary focus of this systematic review and meta-analysis was to evaluate the effects of acute bouts of exercise prior to, during, and following encoding on free-, cued-recall, and recognition episodic memory. PubMed, Scopus, and EBSCO databases were entered, and 42 experiments were subject to meta-analysis. Exercise prior to encoding improved memory (d = 0.23) and affected free-recall (d = 0.40) tests of memory more than cued-recall (d = 0.08) or recognition (d = −0.06) memory. Exercise following encoding improved memory (d = 0.33) and affected recognition (d = 0.62) memory more than free- (d = 0.19) or cued-recall (d = 0.14) memory. Exercise during encoding did not influence memory (d = −0.04). Moderator analyses revealed that exercise before encoding impacted memory differentially on the basis of age, exercise type, and test-timing. When exercise occurred after encoding, age and exercise type, but not timing of the test influenced memory performance. Exercise before and after encoding has selective effects on episodic memory. Additional experiments that evaluate how bouts of exercise influence memory encoding are warranted.
Systematic review registration
PROSPERO, identifier CRD42020202784.
... Biological neural networks exhibit apparent advantages via the Complementary Learning Systems (CLS) [10,13]. In CLS, the Hippocampus rapidly encodes task data and then consolidates the task knowledge into the Cortex by forming new neural connections. ...
Neural networks encounter the challenge of Catastrophic Forgetting (CF) in continual learning, where new task learning interferes with previously learned knowledge. Existing data fine-tuning and regularization methods necessitate task identity information during inference and cannot eliminate interference among different tasks, while soft parameter sharing approaches encounter the problem of an increasing model parameter size. To tackle these challenges, we propose the Remembering Transformer, inspired by the brain's Complementary Learning Systems (CLS). Remembering Transformer employs a mixture-of-adapters architecture and a generative model-based novelty detection mechanism in a pretrained Transformer to alleviate CF. Remembering Transformer dynamically routes task data to the most relevant adapter with enhanced parameter efficiency based on knowledge distillation. We conducted extensive experiments, including ablation studies on the novelty detection mechanism and model capacity of the mixture-of-adapters, in a broad range of class-incremental split tasks and permutation tasks. Our approach demonstrated SOTA performance surpassing the second-best method by 15.90% in the split tasks, reducing the memory footprint from 11.18M to 0.22M in the five splits CIFAR10 task.
... Memory consolidation, a process that stabilizes a memory trace after its initial acquisition, is crucial in both classical and operant conditioning and observational learning. This process involves transferring information from short-term to long-term memory, which is believed to occur primarily during sleep (McGaugh, 2000). ...
This literature review embarks on a detailed exploration of the neurobiological underpinnings that facilitate learning and memory, unraveling the complexities of the brain's mechanisms in these processes. It delves into the critical roles played by neural structures such as the hippocampus, amygdala, and prefrontal cortex, alongside the essential contributions of neurotransmitters, including glutamate, acetylcholine, and dopamine. Synaptic plasticity, focusing on Long-Term Potentiation (LTP) and Long-Term Depression (LTD), is thoroughly examined to understand the strengthening and weakening of neural connections to learning and memory. The review adopts a comprehensive approach by integrating cognitive and behavioral neuroscience perspectives, scrutinizing models of information processing and the sequential processes of encoding, storage, and retrieval. It also evaluates the application of classical and operant conditioning paradigms in understanding memory mechanisms. A critical examination of research methodologies is presented, highlighting the use of neuroimaging techniques such as fMRI, PET, and EEG and discussing experimental designs in human and animal studies to offer an in-depth overview of investigative strategies in this domain. Further, the review explores significant advancements in memory research, including memory enhancement techniques, cognitive training, neurofeedback, and pharmacological interventions, and discusses their implications for education and clinical practice. It addresses memory pathologies, such as Alzheimer's disease and dementia, to understand their effects on learning processes. The review extends its implications to educational applications, discussing evidence-based teaching strategies and clinical applications and exploring therapeutic interventions for memory-related disorders. Concluding with a forward-looking perspective, the review touches on emerging technologies, ethical considerations, and the potential for interdisciplinary research, suggesting new pathways for exploration. By synthesizing key findings and reflecting on the current state of neuroscience in learning and memory, this literature review sets the stage for future research directions, aiming to deepen our understanding of how we acquire, retain, and recall information
... • Memory Consolidation: Memory consolidation is the process by which memories are stabilized and strengthened over time. It involves the transfer of information from short-term memory to long-term memory through processes such as rehearsal, elaboration, and sleepdependent consolidation (McGaugh, 2000). ...
This paper delves into the intricate interplay between artificial intelligence (AI), human memory, and spiritual development, aiming to uncover their interconnectedness and potential synergies in enhancing cognitive understanding and personal growth. Firstly, it comprehensively explores the concept of human memory, including its definition, function, processes, and stages, while outlining a comprehensive design to elucidate its workings. Secondly, it examines the complex relationship between memory and intelligence, highlighting various cognitive processes and factors involved. Thirdly, it conducts a detailed analysis of the physiological mechanisms underlying human memory, with a focus on glucose metabolism, oxygen supply, and nutritional factors, supported by scientific evidence and examples. Furthermore, it explores the spiritual dimensions of human memory, investigating the source of the power that establishes spiritual connections within memory processes. Finally, it examines the interconnectedness between AI, human memory, and spiritual development, elucidating their interactions and potential synergies in fostering cognitive understanding and personal growth. The qualitative study used interviews and group discussions to explore human memory’s complexity and its links with intelligence, physiology, spirituality, and AI. Fifty participants shared diverse insights, guiding discussions on memory and spirituality. The comprehensive exploration of human memory uncovers intricate processes and mechanisms. Spiritual power, often overlooked, shapes memory function, influencing cognitive development and emotional resilience. Integrating spiritual aspects enriches understanding, fostering self-discovery and alignment with higher selves.
... Neurons and synapses constitute the fundamental components of natural neural systems. 4,46,47 In the neural system, the information transfer relies on the synapse structure between two neurons (pre-and postsynaptic neurons) as depicted in Figure 6a. Neurobiologically, synaptic weights can be changed in response to external stimulations. ...
In response to the growing need for efficient processing of temporal information, neuromorphic computing systems are placing increased emphasis on the switching dynamics of memristors. While the switching dynamics can be regulated by the properties of input signals, the ability of controlling it via electrolyte properties of a memristor is essential to further enrich the switching states and improve data processing capability. This study presents the synthesis of mesoporous silica (mSiO2) films using a sol–gel process, which enables the creation of films with controllable porosities. These films can serve as electrolyte layers in the diffusive memristors and lead to tunable neuromorphic switching dynamics. The mSiO2 memristors demonstrate short-term plasticity, which is essential for temporal signal processing. As porosity increases, discernible changes in operating currents, facilitation ratios, and relaxation times are observed. The underlying mechanism of such systematic control was investigated and attributed to the modulation of hydrogen-bonded networks within the porous structure of the silica layer, which significantly influences both anodic oxidation and ion migration processes during switching events. The result of this work presents mesoporous silica as a unique platform for precise control of neuromorphic switching dynamics in diffusive memristors.
