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Learning & Memory (Cold Spring Harbor,... Oct 2019This paper examines recent evidence from behavioral and neuroscience research with nonhuman animals that suggests the intriguing possibility that they, like their human... (Review)
Review
This paper examines recent evidence from behavioral and neuroscience research with nonhuman animals that suggests the intriguing possibility that they, like their human counterparts, are vulnerable to creating false memories. Once considered a uniquely human memory phenomenon, the creation of false memories in lower animals can be seen especially readily in studies involving memory for source, or contextual attributes. Furthermore, evidence of "implanted" misinformation has also been obtained. Here, we review that research and consider its relevance to our empirical understanding of false memories, as well as speculate about its potential clinical implications for trauma memory.
Topics: Animals; Memory, Episodic; Mental Recall; Sex Characteristics
PubMed: 31527184
DOI: 10.1101/lm.050054.119 -
Neuropsychologia Nov 2012Dual-process models of recognition memory distinguish between the retrieval of qualitative information about a prior event (recollection), and judgments of prior... (Review)
Review
Dual-process models of recognition memory distinguish between the retrieval of qualitative information about a prior event (recollection), and judgments of prior occurrence based on an acontextual sense of familiarity. fMRI studies investigating the neural correlates of memory encoding and retrieval conducted within the dual-process framework have frequently reported findings consistent with the view that the hippocampus selectively supports recollection, and has little or no role in familiarity-based recognition. An alternative interpretation of these findings has been proposed, however, in which it is argued that the hippocampus supports the encoding and retrieval of 'strong' memories, regardless of whether the memories are recollection- or familiarity-based. Here, we describe the findings of eight fMRI studies from our laboratory: one study of source memory encoding, four studies of the retrieval of contextual information, and three studies of continuous recognition. Together, the findings support the proposal that hippocampal activity co-varies with the amount of contextual information about a study episode that is encoded or retrieved, and not with the strength of an undifferentiated memory signal.
Topics: Hippocampus; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging; Memory; Mental Processes; Mental Recall
PubMed: 22732490
DOI: 10.1016/j.neuropsychologia.2012.06.004 -
The European Journal of Neuroscience Aug 2019Drug addiction is an aberrant memory that shares the same memory processes as other memories. Brief exposure to drug-associated cues could result in reconsolidation, a... (Review)
Review
Drug addiction is an aberrant memory that shares the same memory processes as other memories. Brief exposure to drug-associated cues could result in reconsolidation, a hypothetical process during which original memory could be updated. In contrast, longer exposure times to drug-associated cues could trigger extinction, a process that decreases the conditioned responding. In this review, we discuss the pharmacological and non-pharmacological manipulations on the reconsolidation and extinction that could be used to interfere with drug reward memories. Pharmacological agents such as β-adrenergic receptor antagonist propranolol can interfere with reconsolidation to disrupt drug reward memory. Pharmacological agents such as the NMDA receptor glycine site agonists d-cycloserine and d-serine can facilitate extinction and then attenuate the expression of drug reward memory. Besides pharmacological interventions, drug-free behavioral approaches by utilizing the reconsolidation and extinction, such as 'post-retrieval extinction' and 'UCS-retrieval extinction', are also effective to erase or inhibit the recall of drug reward memory. Taken together, pharmacological modulation and non-pharmacological modulation of reconsolidation and extinction are promising approaches to regulate drug reward memory and prevent relapse.
Topics: Adrenergic beta-Antagonists; Animals; Conditioning, Classical; Extinction, Psychological; Humans; Memory; Mental Recall; Reward; Substance-Related Disorders
PubMed: 30113098
DOI: 10.1111/ejn.14072 -
Scientific Reports Aug 2023Our brain's capacity for memory storage may be vast but is still finite. Given that we cannot remember the entirety of our experiences, how does our brain select what to...
Our brain's capacity for memory storage may be vast but is still finite. Given that we cannot remember the entirety of our experiences, how does our brain select what to remember and what to forget? Much like the triage of a hospital's emergency room, where urgent cases are prioritized and less critical patients receive delayed or even no care, the brain is believed to go through a similar process of memory triage. Recent salient memories are prioritized for consolidation, which helps create stable, long-term representations in the brain; less salient memories receive a lower priority, and are eventually forgotten if not sufficiently consolidated (Stickgold and Walker in Nat Neurosci 16(2):139-145, 2013). While rodents are a primary model for studying memory consolidation, common behavioral tests typically rely on a limited number of items or contexts, well within the memory capacity of the subject. A memory test allowing us to exceed an animal's memory capacity is key to investigating how memories are selectively strengthened or forgotten. Here we report a new serial novel object recognition task designed to measure memory capacity and prioritization, which we test and validate using female mice.
Topics: Female; Animals; Mice; Brain; Mental Recall; Emergency Service, Hospital; Memory; Memory Consolidation
PubMed: 37640740
DOI: 10.1038/s41598-023-40976-y -
The Neuroscientist : a Review Journal... Jun 2024The brain is designed not only with molecules and cellular processes that help to form memories but also with molecules and cellular processes that suppress the... (Review)
Review
The brain is designed not only with molecules and cellular processes that help to form memories but also with molecules and cellular processes that suppress the formation and retention of memory. The latter processes are critical for an efficient memory management system, given the vast amount of information that each person experiences in their daily activities and that most of this information becomes irrelevant with time. Thus, efficiency dictates that the brain should have processes for selecting the most critical information for storage and suppressing the irrelevant or forgetting it later should it escape the initial filters. Such memory suppressor molecules and processes are revealed by genetic or pharmacologic insults that lead to enhanced memory expression. We review here the predominant memory suppressor molecules and processes that have recently been discovered. They are diverse, as expected, because the brain is complex and employs many different strategies and mechanisms to form memories. They include the gene-repressive actions of small noncoding RNAs, repressors of protein synthesis, cAMP-mediated gene expression pathways, inter- and intracellular signaling pathways for normal forgetting, and others. A deep understanding of memory suppressor molecules and processes is necessary to fully comprehend how the brain forms, stabilizes, and retrieves memories and to reveal how brain disorders disrupt memory.
Topics: Animals; Humans; Brain; Memory; Signal Transduction
PubMed: 36524276
DOI: 10.1177/10738584221138527 -
Frontiers in Neural Circuits 2022Functions of the brain and body are oscillatory in nature and organized according to a logarithmic scale. Brain oscillations and bodily functions such as respiration and...
Functions of the brain and body are oscillatory in nature and organized according to a logarithmic scale. Brain oscillations and bodily functions such as respiration and heartbeat appear nested within each other and coupled together either based on phase or based on phase and amplitude. This facilitates communication in wide-spread neuronal networks and probably also between the body and the brain. It is a widely accepted view, that nested electrophysiological brain oscillations involving the neocortex, thalamus, and the hippocampus form the basis of memory consolidation. This applies especially to declarative memories, that is, memories of life events, for example. Here, we present our view of hippocampal contribution to the process of memory consolidation based on the general ideas stated above and on some recent findings on the topic by us and by other research groups. We propose that in addition to the interplay between neocortical slow oscillations, spindles, and hippocampal sharp-wave ripples during sleep, there are also additional mechanisms available in the hippocampus to control memory consolidation: a rather non-oscillatory hippocampal electrophysiological phenomenon called the dentate spike might provide a means to not only consolidate but to also modify the neural representation of declarative memories. Further, we suggest that memory consolidation in the hippocampus might be in part paced by breathing. These considerations might open new possibilities for regulating memory consolidation in rest and sleep.
Topics: Hippocampus; Memory; Memory Consolidation; Neocortex; Sleep
PubMed: 35431819
DOI: 10.3389/fncir.2022.885684 -
Neuropsychopharmacology Reports Jun 2021The consolidation of short-term memories into long-term memories is promoted by associations with novel environmental stimuli. This phenomenon is known as behavioral...
AIM
The consolidation of short-term memories into long-term memories is promoted by associations with novel environmental stimuli. This phenomenon is known as behavioral tagging. Neuropsin, a plasticity-related serine protease in the hippocampus and amygdala, is involved in memory formation. This study investigated how neuropsin affects associative long-term memory.
METHODS
Short-term and long-term memory were assessed in control and neuropsin-deficient mice by investigating their performance in inhibitory avoidance and spatial object recognition tasks. The effect of exposure to novelty on the conversion of short-term memory to associative long-term memory was also examined.
RESULTS
The consolidation of task-related short-term memories into long-term memories was facilitated by exposing the animals to a novel environment 1 hour before training. However, this long-term memory conversion was impaired in neuropsin-deficient mice performing the inhibitory avoidance task but not the spatial object recognition task.
CONCLUSION
Behavioral tagging occurs via neuropsin-dependent and neuropsin-independent processes for different behavioral tasks.
Topics: Animals; Hippocampus; Memory, Long-Term; Memory, Short-Term; Mice; Rats; Rats, Wistar
PubMed: 33773089
DOI: 10.1002/npr2.12177 -
Learning & Memory (Cold Spring Harbor,... May 2024Drug addiction and the circuitry for learning and memory are intimately intertwined. Drugs of abuse create strong, inappropriate, and lasting memories that contribute to... (Review)
Review
Drug addiction and the circuitry for learning and memory are intimately intertwined. Drugs of abuse create strong, inappropriate, and lasting memories that contribute to many of their destructive properties, such as continued use despite negative consequences and exceptionally high rates of relapse. Studies in are helping us understand how drugs of abuse, especially alcohol, create memories at the level of individual neurons and in the circuits where they function. is a premier organism for identifying the mechanisms of learning and memory. also respond to drugs of abuse in ways that remarkably parallel humans and rodent models. An emerging consensus is that, for alcohol, the mushroom bodies participate in the circuits that control acute drug sensitivity, not explicitly associative forms of plasticity such as tolerance, and classical associative memories of their rewarding and aversive properties. Moreover, it is becoming clear that drugs of abuse use the mushroom body circuitry differently from other behaviors, potentially providing a basis for their addictive properties.
Topics: Animals; Memory; Mushroom Bodies; Learning; Substance-Related Disorders; Drosophila melanogaster; Humans; Drosophila; Illicit Drugs
PubMed: 38862166
DOI: 10.1101/lm.053815.123 -
Journal of Cognitive Neuroscience Nov 2022Although storage in working memory (WM) can be tracked via measurements of ongoing neural activity, past work has shown that observers can maintain access to that...
Although storage in working memory (WM) can be tracked via measurements of ongoing neural activity, past work has shown that observers can maintain access to that information despite temporary interruptions of those neural patterns. This observation has been regarded as evidence for a neurally silent form of WM storage. Alternatively, however, unattended information could be retrieved from episodic long-term memory (eLTM) rather than being maintained in WM during the activity-silent period. Here, we tested between these possibilities by examining whether WM performance showed evidence of proactive interference (PI)-a hallmark of retrieval from eLTM-following such interruptions. Participants remembered the colors (Experiments 1-3) or locations (Experiment 4) of serially presented objects. We found PI for set sizes larger than 4, but not for smaller set sizes, suggesting that eLTM may have supported performance when WM capacity was exceeded. Critically, performance with small set sizes remained resistant to PI, even following prolonged interruptions by a challenging distractor task. Thus, we found evidence for PI-resistant memories that were maintained across likely interruptions of storage-related neural activity, an empirical pattern that implies activity-silent storage in WM.
Topics: Humans; Memory, Short-Term; Memory, Long-Term; Mental Recall
PubMed: 36122353
DOI: 10.1162/jocn_a_01917 -
Neuropsychopharmacology : Official... Mar 2015Emotional and traumatic experiences lead to the development of particularly strong memories that can drive neuropsychiatric disorders, such as posttraumatic stress... (Review)
Review
Emotional and traumatic experiences lead to the development of particularly strong memories that can drive neuropsychiatric disorders, such as posttraumatic stress disorder (PTSD) and drug addiction. Disruption of these memories would therefore serve as a powerful treatment option, and targeting the pathologic emotional, but not declarative, component of a memory would be ideal for clinical intervention. Research reveals that after retrieval of a consolidated memory, the memory can be destabilized, and must then be reconsolidated through synaptic plasticity to allow subsequent retrieval. Disruption of reconsolidation-related plasticity would therefore impair specific, reactivated memories. Noradrenergic signaling strengthens synaptic plasticity and is essential for encoding the emotional components of memory. Consistent with this, investigations have now revealed that noradrenergic signaling is a critical mechanism for reconsolidation of emotional memories in rodent and human models. Here, we discuss these investigations and promising clinical trials indicating that disruption of noradrenergic signaling during reconsolidation may abolish the pathologic emotional, but not declarative, component of memories allowing alleviation of neuropsychiatric disorders including PTSD and drug addiction.
Topics: Animals; Fear; Humans; Memory; Norepinephrine; Signal Transduction
PubMed: 25315025
DOI: 10.1038/npp.2014.243