scholarly journals Evidence of Maintenance Tagging in the Hippocampus for the Persistence of Long-Lasting Memory Storage

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Micol Tomaiuolo ◽  
Cynthia Katche ◽  
Haydee Viola ◽  
Jorge H. Medina
Keyword(s):  
Time Window ◽  
Dorsal Hippocampus ◽  
Training Session ◽  
Critical Time ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Long Term Memory ◽  
Memory Persistence ◽  
Synaptic Tagging And Capture

The synaptic tagging and capture (STC) hypothesis provides a compelling explanation for synaptic specificity and facilitation of long-term potentiation. Its implication on long-term memory (LTM) formation led to postulate the behavioral tagging mechanism. Here we show that a maintenance tagging process may operate in the hippocampus late after acquisition for the persistence of long-lasting memory storage. The proposed maintenance tagging has several characteristics: (1) the tag is transient and time-dependent; (2) it sets in a late critical time window after an aversive training which induces a short-lasting LTM; (3) exposing rats to a novel environment specifically within this tag time window enables the consolidation to a long-lasting LTM; (4) a familiar environment exploration was not effective; (5) the effect of novelty on the promotion of memory persistence requires dopamine D1/D5 receptors and Arc expression in the dorsal hippocampus. The present results can be explained by a broader version of the behavioral tagging hypothesis and highlight the idea that the durability of a memory trace depends either on late tag mechanisms induced by a training session or on events experienced close in time to this tag.

scholarly journals The Longevity of Hippocampus-Dependent Memory Is Orchestrated by the Locus Coeruleus-Noradrenergic System

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Niels Hansen
Keyword(s):  
Locus Coeruleus ◽  
Transcriptional Control ◽  
Dorsal Hippocampus ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Long Term Memory ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Hippocampus Dependent Memory

The locus coeruleus is connected to the dorsal hippocampus via strong fiber projections. It becomes activated after arousal and novelty, whereupon noradrenaline is released in the hippocampus. Noradrenaline from the locus coeruleus is involved in modulating the encoding, consolidation, retrieval, and reversal of hippocampus-based memory. Memory storage can be modified by the activation of the locus coeruleus and subsequent facilitation of hippocampal long-term plasticity in the forms of long-term depression and long-term potentiation. Recent evidence indicates that noradrenaline and dopamine are coreleased in the hippocampus from locus coeruleus terminals, thus fostering neuromodulation of long-term synaptic plasticity and memory. Noradrenaline is an inductor of epigenetic modifications regulating transcriptional control of synaptic long-term plasticity to gate the endurance of memory storage. In conclusion, locus coeruleus activation primes the persistence of hippocampus-based long-term memory.

scholarly journals Critical Time-Window for NO–cGMP-Dependent Long-Term Memory Formation after One-Trial Appetitive Conditioning

2002 ◽  
Vol 22 (4) ◽  
pp. 1414-1425 ◽  
Author(s):  
Ildikó Kemenes ◽  
György Kemenes ◽  
Richard J. Andrew ◽  
Paul R. Benjamin ◽  
Michael O'Shea
Keyword(s):  
Time Window ◽  
Critical Time ◽  
Memory Formation ◽  
Long Term Memory ◽  
Appetitive Conditioning ◽  
Term Memory

scholarly journals Gradation (approx. 10 size states) of synaptic strength by quantal addition of structural modules

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160328 ◽  
Author(s):  
Kang K. L. Liu ◽  
Michael F. Hagan ◽  
John E. Lisman
Keyword(s):  
Functional Module ◽  
Late Phase ◽  
Matrix Material ◽  
Super Resolution ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Homeostatic Plasticity ◽  
Memory Storage ◽  
Long Term Memory

Memory storage involves activity-dependent strengthening of synaptic transmission, a process termed long-term potentiation (LTP). The late phase of LTP is thought to encode long-term memory and involves structural processes that enlarge the synapse. Hence, understanding how synapse size is graded provides fundamental information about the information storage capability of synapses. Recent work using electron microscopy (EM) to quantify synapse dimensions has suggested that synapses may structurally encode as many as 26 functionally distinct states, which correspond to a series of proportionally spaced synapse sizes. Other recent evidence using super-resolution microscopy has revealed that synapses are composed of stereotyped nanoclusters of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and scaffolding proteins; furthermore, synapse size varies linearly with the number of nanoclusters. Here we have sought to develop a model of synapse structure and growth that is consistent with both the EM and super-resolution data. We argue that synapses are composed of modules consisting of matrix material and potentially one nanocluster. LTP induction can add a trans-synaptic nanocluster to a module, thereby converting a silent module to an AMPA functional module. LTP can also add modules by a linear process, thereby producing an approximately 10-fold gradation in synapse size and strength. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

scholarly journals Metaplasticity mechanisms restore plasticity and associativity in an animal model of Alzheimer’s disease

2017 ◽  
Vol 114 (21) ◽  
pp. 5527-5532 ◽  
Author(s):  
Qin Li ◽  
Sheeja Navakkode ◽  
Martin Rothkegel ◽  
Tuck Wah Soong ◽  
Sreedharan Sajikumar ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Ryanodine Receptors ◽  
Long Term Potentiation ◽  
Neuronal Population ◽  
Memory Storage ◽  
Dynamic Regulation ◽  
Model Of Alzheimer’S Disease ◽  
Synaptic Tagging And Capture

Dynamic regulation of plasticity thresholds in a neuronal population is critical for the formation of long-term plasticity and memory and is achieved by mechanisms such as metaplasticity. Metaplasticity tunes the synapses to undergo changes that are necessary prerequisites for memory storage under physiological and pathological conditions. Here we discovered that, in amyloid precursor protein (APP)/presenilin-1 (PS1) mice (age 3–4 mo), a prominent mouse model of Alzheimer’s disease (AD), late long-term potentiation (LTP; L-LTP) and its associative plasticity mechanisms such as synaptic tagging and capture (STC) were impaired already in presymptomatic mice. Interestingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associative interaction of LTP and LTD, cross-capture, was altered in these mice. Metaplastic activation of ryanodine receptors (RyRs) in these neurons reestablished L-LTP and STC. We propose that RyR-mediated metaplastic mechanisms can be considered as a possible therapeutic target for counteracting synaptic impairments in the neuronal networks during the early progression of AD.

scholarly journals Early β adrenoceptor dependent time window for fear memory persistence in APPswe/PS1dE9 mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Smitha Karunakaran
Keyword(s):  
Fear Conditioning ◽  
Time Window ◽  
Fear Memory ◽  
Long Term Memory ◽  
Term Memory ◽  
Contextual Fear ◽  
Adrenoceptor Agonist ◽  
Hippocampal Ca1 ◽  
Memory Persistence

AbstractIn this study we demonstrate that 2 month old APPswe/PS1dE9 mice, a transgenic model of Alzheimer’s disease, exhibited intact short-term memory in Pavlovian hippocampal—dependent contextual fear learning task. However, their long-term memory was impaired. Intra-CA1 infusion of isoproterenol hydrochloride, the β-adrenoceptor agonist, to the ventral hippocampus of APPswe/PS1dE9 mice immediately before fear conditioning restored long-term contextual fear memory. Infusion of the β-adrenoceptor agonist + 2.5 h after fear conditioning only partially rescued the fear memory, whereas infusion at + 12 h post conditioning did not interfere with long-term memory persistence in this mouse model. Furthermore, Intra-CA1 infusion of propranolol, the β-adrenoceptor antagonist, administered immediately before conditioning to their wildtype counterpart impaired long-term fear memory, while it was ineffective when administered + 4 h and + 12 h post conditioning. Our results indicate that, long-term fear memory persistence is determined by a unique β-adrenoceptor sensitive time window between 0 and + 2.5 h upon learning acquisition, in the ventral hippocampal CA1 of APPswe/PS1dE9 mice. On the contrary, β-adrenoceptor agonist delivery to ventral hippocampal CA1 per se did not enhance innate anxiety behaviour in open field test. Thus we conclude that, activation of learning dependent early β-adrenoceptor modulation underlies and is necessary to promote long-term fear memory persistence in APPswe/PS1dE9.

Protein Synthesis and Synapse Specificity in Functional Plasticity

2019 ◽  
Author(s):  
Radha Raghuraman ◽  
Amrita Benoy ◽  
Sreedharan Sajikumar
Keyword(s):  
Protein Synthesis ◽  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Synaptic Activity ◽  
Long Term Memory ◽  
Term Potentiation ◽  
Synaptic Tagging And Capture ◽  
Dendritic Protein Synthesis ◽  
Related Proteins

This chapter discusses the role of protein synthesis in the maintenance of long-term potentiation (LTP) and its associative properties, synaptic tagging and capture, which are cellular correlates of long-term memory. Starting from a brief overview of the early and late phases of LTP, the chapter discusses various existing models for synaptic activity-induced protein synthesis and its roles in late-LTP. The synaptic tagging and capture and cross-tagging theories are given emphasis, along with the elucidation of local dendritic protein synthesis and its significance in the maintenance of LTP. Inverse synaptic tagging, synaptic competition for plasticity-related proteins, and metaplasticity are also covered. The importance of the balance between proteasomal degradation and synthesis of plasticity-related proteins in persistent potentiation is briefly discussed. This chapter touches upon the physiological implications of epigenetic regulation in the control of neuronal functions and the molecular mechanisms within the neurons that translate epigenetic changes into long-lasting responses.

scholarly journals Delayed wave of c-Fos expression in the dorsal hippocampus involved specifically in persistence of long-term memory storage

2009 ◽  
Vol 107 (1) ◽  
pp. 349-354 ◽  
Author(s):  
C. Katche ◽  
P. Bekinschtein ◽  
L. Slipczuk ◽  
A. Goldin ◽  
I. A. Izquierdo ◽  
...  
Keyword(s):  
Dorsal Hippocampus ◽  
Memory Storage ◽  
Long Term Memory ◽  
Term Memory ◽  
Fos Expression

scholarly journals Integrated Overview of the Memory System

2021 ◽  
Vol 9 (VI) ◽  
pp. 3328-3338
Author(s):  
Ishanee Das Sharma
Keyword(s):  
Molecular Mechanisms ◽  
Short Term Memory ◽  
Long Term Potentiation ◽  
Point Of View ◽  
Memory Storage ◽  
Long Term Memory ◽  
Special Focus ◽  
Term Memory ◽  
Term Potentiation

This review aims to clarify and classify memory from psychological and neuroscientific point of view, delving into the molecular mechanisms taking place as well. The main forms of memory are sensory memory, short term memory and long-term memory. We also try to specify the flow of information through various memory models. The concept of synaptic plasticity and long-term potentiation is highlighted, with special focus on the physiological parts of the brain that are involved in memory storage. Overall, this study will help expand our knowledge on the intrinsic details of memory storage and the functioning of our brain.

scholarly journals PKMζ traces hippocampal LTP maintenance and spatial long-term memory

2020 ◽  
Author(s):  
Changchi Hsieh ◽  
Panayiotis Tsokas ◽  
Ain Chung ◽  
Claudia Garcia-Jou ◽  
Edith Lesburguères ◽  
...  
Keyword(s):  
Fluorescent Protein ◽  
Hippocampal Formation ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Long Term Memory ◽  
Term Memory ◽  
Ca1 Pyramidal Cells

PKMζ is an autonomously active, atypical PKC isoform crucial for maintaining synaptic long-term potentiation (LTP) and long-term memory. Unlike other PKCs that are transiently activated by short-lived second messengers, PKMζ is persistently activated by long-lasting increases in the amount of the autonomously active kinase during LTP and long-term memory maintenance. Thus, localizing persistent increases in PKMζ might reveal traces of physiological LTP maintenance in the circuitry of the brain during long-term memory storage. Using quantitative immunohistochemistry validated by the lack of staining in PKMζ-null mice, we visualized the amount and distribution of PKMζ during LTP maintenance and spatial long-term memory storage in the hippocampal formation of wild-type mice. Strong afferent stimulation of Schaffer collateral/commissural fibers inducing LTP maintenance increases PKMζ in CA1 pyramidal cells for 2 hours in hippocampal slices. Active place avoidance spatial conditioning increases PKMζ in CA1 pyramidal cells of the hippocampal formation from 1 day to at least 1 month. The increases in PKMζ coincide with the location of cells marked during long-term memory training by Arc promoter-mediated expression of a fluorescent protein, including at dendritic spines. We conclude that increased PKMζ forms persistent traces in CA1 pyramidal cells that are sites of molecular information storage during LTP maintenance and spatial long-term memory.Graphical AbstractPKMζ-immunohistochemistry reveals persistent increased PKMζ in the hippocampus during (A) LTP maintenance, and (B) spatial long-term memory storage.

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