scholarly journals Neural correlates of episodic memory modulated by temporally delayed rewards

2019 ◽  
Author(s):  
Jungsun Yoo ◽  
Seokyoung Min ◽  
Seung-Koo Lee ◽  
Sanghoon Han
Keyword(s):  
Memory Performance ◽  
Long Term Potentiation ◽  
Neural Correlates ◽  
Temporal Distance ◽  
Long Term Memory ◽  
Memory Encoding ◽  
Term Potentiation ◽  
Subjective Value ◽  
Behavioral Memory

AbstractWhen a stimulus is associated with an external reward, its chance of being consolidated into long-term memory is boosted via dopaminergic facilitation of long-term potentiation in the hippocampus. Given that higher temporal distance (TD) has been found to discount the subjective value of a reward, we hypothesized that memory performance associated with a more immediate reward will result in better memory performance. We tested this hypothesis by measuring both behavioral memory performance and brain activation using functional magnetic resonance imaging (fMRI) during memory encoding and retrieval tasks. Contrary to our hypothesis, both behavioral and fMRI results suggest that the TD of rewards might enhance the chance of the associated stimulus being remembered. The fMRI data demonstrate that the lateral prefrontal cortex, which shows encoding-related activation proportional to the TD, is reactivated when searching for regions that show activation proportional to the TD during retrieval. This is not surprising given that this region is not only activated to discriminate between future vs. immediate rewards, it is also a part of the retrieval-success network. These results provide support for the conclusion that the encoding-retrieval overlap provoked as the rewards are more delayed lead to better memory performance of the items associated with the rewards.

scholarly journals Neural correlates of episodic memory modulated by temporally delayed rewards

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249290
Author(s):  
Jungsun Yoo ◽  
Seokyoung Min ◽  
Seung-Koo Lee ◽  
Sanghoon Han
Keyword(s):  
Memory Performance ◽  
Long Term Potentiation ◽  
Neural Correlates ◽  
Temporal Distance ◽  
Long Term Memory ◽  
Memory Encoding ◽  
Term Potentiation ◽  
Subjective Value ◽  
Behavioral Memory

When a stimulus is associated with an external reward, its chance of being consolidated into long-term memory is boosted via dopaminergic facilitation of long-term potentiation in the hippocampus. Given that higher temporal distance (TD) has been found to discount the subjective value of a reward, we hypothesized that memory performance associated with a more immediate reward will result in better memory performance. We tested this hypothesis by measuring both behavioral memory performance and brain activation using functional magnetic resonance imaging (fMRI) during memory encoding and retrieval tasks. Contrary to our hypothesis, both behavioral and fMRI results suggest that the TD of rewards might enhance the chance of the associated stimulus being remembered. The fMRI data demonstrate that the lateral prefrontal cortex, which shows encoding-related activation proportional to the TD, is reactivated when searching for regions that show activation proportional to the TD during retrieval. This is not surprising given that this region is not only activated to discriminate between future vs. immediate rewards, it is also a part of the retrieval-success network. These results provide support for the conclusion that the encoding-retrieval overlap provoked as the rewards are more delayed may lead to better memory performance of the items associated with the rewards.

scholarly journals Human sensory Long-Term Potentiation (LTP) predicts visual memory performance and is modulated by the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism

2018 ◽  
Author(s):  
M.J. Spriggs ◽  
C.S. Thompson ◽  
D Moreau ◽  
N.A. McNair ◽  
C.C. Wu ◽  
...  
Keyword(s):  
Visual Memory ◽  
Memory Performance ◽  
Memory Function ◽  
Human Memory ◽  
Long Term Potentiation ◽  
Long Term Memory ◽  
Term Memory ◽  
Term Potentiation ◽  
The Relationship

BackgroundLong-Term Potentiation (LTP) is recognised as a core neuronal process underlying long-term memory. However, a direct relationship between LTP and human memory performance is yet to be demonstrated. The first aim of the current study was thus to assess the relationship between LTP and human long-term memory performance. With this also comes an opportunity to explore factors thought to mediate the relationship between LTP and long-term memory, and to gain additional insight into variations in memory function and memory decline. The second aim of the current study was to explore the relationship between LTP and memory in groups differing with respect to BDNF Val66Met; a single nucleotide polymorphism implicated in memory function.Methods28 participants (15 female) were split into three genotype groups (Val/Val, Val/Met, Met/Met) and were presented with both an EEG paradigm for inducing LTP-like enhancements of the visually-evoked response, and a test of visual memory.ResultsThe magnitude of LTP 40 minutes after induction was predictive of long-term memory performance. Additionally, the BDNF Met allele was associated with both reduced LTP and reduced memory performance.ConclusionsThe current study not only presents the first evidence for a relationship between sensory LTP and human memory performance, but also demonstrates how targeting this relationship can provide insight into factors implicated in variation in human memory performance. It is anticipated that this will be of utility to future clinical studies of disrupted memory function.

scholarly journals The immediate early gene Arc is not required for hippocampal long-term potentiation

2020 ◽  
Author(s):  
M. Kyrke-Smith ◽  
L.J. Volk ◽  
S.F. Cooke ◽  
M.F. Bear ◽  
R.L. Huganir ◽  
...  
Keyword(s):  
Immediate Early Gene ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Early Gene ◽  
Immediate Early ◽  
Long Term Memory ◽  
Memory Encoding ◽  
Term Potentiation ◽  
Mrna And Protein Expression

ABSTRACTThe immediate early gene Arc is critical for maintenance of long-term memory. How Arc mediates this process remains unclear, but it has been proposed to sustain Hebbian synaptic potentiation, which is a key component of memory encoding. This form of plasticity is modelled experimentally by induction of long-term potentiation (LTP), which increases Arc mRNA and protein expression. However, mechanistic data implicates Arc in the endocytosis of AMPA-type glutamate receptors and the weakening of synapses. Here, we took a comprehensive approach to determine if Arc is necessary for hippocampal LTP. We find that Arc is not required for LTP maintenance and must regulate memory storage through alternative mechanisms.

scholarly journals Synaptic plasticity-dependent competition rule influences memory formation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yire Jeong ◽  
Hye-Yeon Cho ◽  
Mujun Kim ◽  
Jung-Pyo Oh ◽  
Min Soo Kang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Specific Pattern ◽  
Memory Encoding ◽  
Competition Rule ◽  
Term Potentiation ◽  
Input Activity

AbstractMemory is supported by a specific collection of neurons distributed in broad brain areas, an engram. Despite recent advances in identifying an engram, how the engram is created during memory formation remains elusive. To explore the relation between a specific pattern of input activity and memory allocation, here we target a sparse subset of neurons in the auditory cortex and thalamus. The synaptic inputs from these neurons to the lateral amygdala (LA) are not potentiated by fear conditioning. Using an optogenetic priming stimulus, we manipulate these synapses to be potentiated by the learning. In this condition, fear memory is preferentially encoded in the manipulated cell ensembles. This change, however, is abolished with optical long-term depression (LTD) delivered shortly after training. Conversely, delivering optical long-term potentiation (LTP) alone shortly after fear conditioning is sufficient to induce the preferential memory encoding. These results suggest a synaptic plasticity-dependent competition rule underlying memory formation.

scholarly journals Effects of D‐amino acid oxidase inhibition on memory performance and long‐term potentiation in vivo

2013 ◽  
Vol 1 (1) ◽  
Author(s):  
Seth C. Hopkins ◽  
Una C. Campbell ◽  
Michele L. R. Heffernan ◽  
Kerry L. Spear ◽  
Ross D. Jeggo ◽  
...  
Keyword(s):  
Amino Acid ◽  
Memory Performance ◽  
Long Term Potentiation ◽  
Acid Oxidase ◽  
Amino Acid Oxidase ◽  
Term Potentiation ◽  
Oxidase Inhibition

scholarly journals Deletion of novel protein TMEM35 alters stress-related functions and impairs long-term memory in mice

2016 ◽  
Vol 311 (1) ◽  
pp. R166-R178 ◽  
Author(s):  
Bruce C. Kennedy ◽  
Jiva G. Dimova ◽  
Srikanth Dakoji ◽  
Li-Lian Yuan ◽  
Jonathan C. Gewirtz ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Pathway Analysis ◽  
Transmembrane Protein ◽  
Long Term Potentiation ◽  
Synaptic Proteins ◽  
Molecular Networks ◽  
Long Term Memory ◽  
Term Memory ◽  
Term Potentiation

The mounting of appropriate emotional and neuroendocrine responses to environmental stressors critically depends on the hypothalamic-pituitary-adrenal (HPA) axis and associated limbic circuitry. Although its function is currently unknown, the highly evolutionarily conserved transmembrane protein 35 (TMEM35) is prominently expressed in HPA circuitry and limbic areas, including the hippocampus and amygdala. To investigate the possible involvement of this protein in neuroendocrine function, we generated tmem35 knockout (KO) mice to characterize the endocrine, behavioral, electrophysiological, and proteomic alterations caused by deletion of the tmem35 gene. While capable of mounting a normal corticosterone response to restraint stress, KO mice showed elevated basal corticosterone accompanied by increased anxiety-like behavior. The KO mice also displayed impairment of hippocampus-dependent fear and spatial memories. Given the intact memory acquisition but a deficit in memory retention in the KO mice, TMEM35 is likely required for long-term memory consolidation. This conclusion is further supported by a loss of long-term potentiation in the Schaffer collateral-CA1 pathway in the KO mice. To identify putative molecular pathways underlying alterations in plasticity, proteomic analysis of synaptosomal proteins revealed lower levels of postsynaptic molecules important for synaptic plasticity in the KO hippocampus, including PSD95 and N-methyl-d-aspartate receptors. Pathway analysis (Ingenuity Pathway Analysis) of differentially expressed synaptic proteins in tmem35 KO hippocampus implicated molecular networks associated with specific cellular and behavioral functions, including decreased long-term potentiation, and increased startle reactivity and locomotion. Collectively, these data suggest that TMEM35 is a novel factor required for normal activity of the HPA axis and limbic circuitry.

scholarly journals Bistable MAP kinase activity: a plausible mechanism contributing to maintenance of late long-term potentiation

2008 ◽  
Vol 294 (2) ◽  
pp. C503-C515 ◽  
Author(s):  
Paul Smolen ◽  
Douglas A. Baxter ◽  
John H. Byrne
Keyword(s):  
Map Kinase ◽  
Dendritic Spine ◽  
Mapk Pathway ◽  
Long Term Potentiation ◽  
Long Term Memory ◽  
Stable States ◽  
Mapk Activity ◽  
Stochastic Fluctuations ◽  
Term Potentiation

Bistability of MAP kinase (MAPK) activity has been suggested to contribute to several cellular processes, including differentiation and long-term synaptic potentiation. A recent model (Markevich NI, Hoek JB, Kholodenko BN. J Cell Biol 164: 353–359, 2004) predicts bistability due to interactions of the kinases and phosphatases in the MAPK pathway, without feedback from MAPK to earlier reactions. Using this model and enzyme concentrations appropriate for neurons, we simulated bistable MAPK activity, but bistability was present only within a relatively narrow range of activity of Raf, the first pathway kinase. Stochastic fluctuations in molecule numbers eliminated bistability for small molecule numbers, such as are expected in the volume of a dendritic spine. However, positive-feedback loops have been posited from MAPK up to Raf activation. One proposed loop in which MAPK directly activates Raf was incorporated into the model. We found that such feedback greatly enhanced the robustness of both stable states of MAPK activity to stochastic fluctuations and to parameter variations. Bistability was robust for molecule numbers plausible for a dendritic spine volume. The upper state of MAPK activity was resistant to inhibition of MEK activation for >1 h, which suggests that inhibitor experiments have not sufficed to rule out a role for persistent MAPK activity in the maintenance of long-term potentiation (LTP). These simulations suggest that persistent MAPK activity and consequent upregulation of translation may contribute to LTP maintenance and to long-term memory. Experiments using a fluorescent MAPK substrate may further test this hypothesis.

scholarly journals The evidence for hippocampal long-term potentiation as a basis of memory for simple tasks

2008 ◽  
Vol 80 (1) ◽  
pp. 115-127 ◽  
Author(s):  
Iván Izquierdo ◽  
Martín Cammarota ◽  
Weber C. Da Silva ◽  
Lia R.M. Bevilaqua ◽  
Janine I. Rossato ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Brain Regions ◽  
Memory Formation ◽  
Long Term Memory ◽  
Ca1 Region ◽  
Term Potentiation ◽  
The One ◽  
Similar Task ◽  
Stimulation Of

Long-term potentiation (LTP) is the enhancement of postsynaptic responses for hours, days or weeks following the brief repetitive afferent stimulation of presynaptic afferents. It has been proposed many times over the last 30 years to be the basis of long-term memory. Several recent findings finally supported this hypothesis: a) memory formation of one-trial avoidance learning depends on a series of molecular steps in the CA1 region of the hippocampus almost identical to those of LTP in the same region; b)hippocampal LTP in this region accompanies memory formation of that task and of another similar task. However, CA1 LTP and the accompanying memory processes can be dissociated, and in addition plastic events in several other brain regions(amygdala, entorhinal cortex, parietal cortex) are also necessary for memory formation of the one-trial task, and perhaps of many others.

scholarly journals Endophilin A1 promotes Actin Polymerization in response to Ca2+/calmodulin to Initiate Structural Plasticity of Dendritic Spines

2020 ◽  
Author(s):  
Yanrui Yang ◽  
Jiang Chen ◽  
Xue Chen ◽  
Di Li ◽  
Jianfeng He ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Actin Polymerization ◽  
Morphological Changes ◽  
Structural Plasticity ◽  
Long Term Potentiation ◽  
Membrane Dynamics ◽  
Long Term Memory ◽  
Induction Phase ◽  
Term Potentiation

AbstractDendritic spines of excitatory neurons undergo activity-dependent structural and functional plasticity, which are cellular correlates of learning and memory. However, mechanisms underlying the rapid morphological changes immediately after NMDAR-mediated Ca2+ influx into spines remain poorly understood. Here we report that endophilin A1, a neuronal N-BAR protein, orchestrates membrane dynamics with actin polymerization to initiate spine enlargement in the induction phase of long-term potentiation (LTP). Upon LTP induction, Ca2+/calmodulin enhances its binding to both membrane and p140Cap, a cytoskeleton regulator. As a result, endophilin A1 rapidly associates with the relaxed plasma membrane and promotes actin polymerization, leading to acute expansion of spine head. Moreover, not only the p140Cap-binding, but also calmodulin- and membrane-binding capacities of endophilin A1 are required for LTP and long-term memory. Thus, endophilin A1 functions as calmodulin effector to drive spine enlargement in response to Ca2+ influx in the initial phase of structural plasticity.

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