scholarly journals The synaptic plasticity and memory hypothesis: encoding, storage and persistence

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130288 ◽  
Author(s):  
Tomonori Takeuchi ◽  
Adrian J. Duszkiewicz ◽  
Richard G. M. Morris
Keyword(s):  
Synaptic Plasticity ◽  
Optical Imaging ◽  
Brain Area ◽  
Molecular Genetic ◽  
Memory Formation ◽  
New Work ◽  
Necessary And Sufficient ◽  
Activity Dependent ◽  
The Brain

The synaptic plasticity and memory hypothesis asserts that activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation and is both necessary and sufficient for the encoding and trace storage of the type of memory mediated by the brain area in which it is observed. Criteria for establishing the necessity and sufficiency of such plasticity in mediating trace storage have been identified and are here reviewed in relation to new work using some of the diverse techniques of contemporary neuroscience. Evidence derived using optical imaging, molecular-genetic and optogenetic techniques in conjunction with appropriate behavioural analyses continues to offer support for the idea that changing the strength of connections between neurons is one of the major mechanisms by which engrams are stored in the brain.

scholarly journals Synaptic control of DNA methylation involves activity-dependent degradation of DNMT3A1 in the nucleus

2020 ◽  
Vol 45 (12) ◽  
pp. 2120-2130 ◽  
Author(s):  
Gonca Bayraktar ◽  
PingAn Yuanxiang ◽  
Alessandro D. Confettura ◽  
Guilherme M. Gomes ◽  
Syed A. Raza ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Synaptic Plasticity ◽  
Promoter Methylation ◽  
Dna Methyltransferase ◽  
De Novo ◽  
Memory Formation ◽  
Epigenetic Mark ◽  
Dependent Manner ◽  
Synaptic Control ◽  
Activity Dependent

Abstract DNA methylation is a crucial epigenetic mark for activity-dependent gene expression in neurons. Very little is known about how synaptic signals impact promoter methylation in neuronal nuclei. In this study we show that protein levels of the principal de novo DNA-methyltransferase in neurons, DNMT3A1, are tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subunit. Interestingly, synaptic NMDARs drive degradation of the methyltransferase in a neddylation-dependent manner. Inhibition of neddylation, the conjugation of the small ubiquitin-like protein NEDD8 to lysine residues, interrupts degradation of DNMT3A1. This results in deficits in promoter methylation of activity-dependent genes, as well as synaptic plasticity and memory formation. In turn, the underlying molecular pathway is triggered by the induction of synaptic plasticity and in response to object location learning. Collectively, the data show that plasticity-relevant signals from GluN2A-containing NMDARs control activity-dependent DNA-methylation involved in memory formation.

scholarly journals Reading Memory Formation from the Eyes

2018 ◽  
Author(s):  
Anne Bergt ◽  
Anne E. Urai ◽  
Tobias H. Donner ◽  
Lars Schwabe
Keyword(s):  
Synaptic Plasticity ◽  
Memory Formation ◽  
Pupil Dilation ◽  
Long Term Memory ◽  
Term Memory ◽  
Pupil Response ◽  
Rapid Formation ◽  
The Brain

At any time, we are processing thousands of stimuli, but only few of them will be remembered hours or days later. Is there any way to predict which ones? Here, we show that the pupil response to ongoing stimuli, an indicator of physiological arousal, is a reliable predictor of long-term memory for these stimuli, over at least one day. Pupil dilation was tracked while participants performed visual and auditory encoding tasks. Memory was tested immediately after encoding and 24 hours later. Irrespective of the encoding modality, trial-by-trial variations in pupil dilation predicted which stimuli were recalled in the immediate and 24 hours-delayed tests. These results show that our eyes may provide a window into the formation of long-term memories. Furthermore, our findings underline the important role of central arousal systems in the rapid formation of memories in the brain, possibly by gating synaptic plasticity mechanisms.

scholarly journals Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus

2019 ◽  
Author(s):  
Gonca Bayraktar ◽  
PingAn Yuanxiang ◽  
Guilherme M Gomes ◽  
Aessandro D Confettura ◽  
Syed A Raza ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Synaptic Plasticity ◽  
Promoter Methylation ◽  
Dna Methyltransferase ◽  
De Novo ◽  
Memory Formation ◽  
Epigenetic Mark ◽  
Dependent Manner ◽  
Synaptic Control ◽  
Activity Dependent

AbstractDNA-methylation is a crucial epigenetic mark for activity-dependent gene expression in neurons. Very little is known how synaptic signals impact promoter methylation in neuronal nuclei. In this study we show that protein levels of the principal de novo DNA-methyltransferase in neurons, DNMT3a1, are tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subunit. Interestingly, synaptic NMDAR drive degradation of the methyltransferase in a neddylation-dependent manner. Inhibition of neddylation, the conjugation of the small ubiquitin-like protein NEDD8 to lysine residues, interrupts degradation of DNMT3a1 and results in deficits of promoter methylation of activity-dependent genes, synaptic plasticity as well as memory formation. In turn, the underlying molecular pathway is triggered by the induction of synaptic plasticity and in response to object location learning. Collectively the data show that GluN2A containing NMDAR control synapse-to-nucleus signaling that links plasticity-relevant signals to activity-dependent DNA-methylation involved in memory formation.

scholarly journals Molekulare Regulation der neuronalen Plastizität und Lernprozesse

BIOspektrum ◽  
2020 ◽  
Vol 26 (6) ◽  
pp. 600-602
Author(s):  
Marta Zagrebelsky
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Neuronal Plasticity ◽  
Neuronal Networks ◽  
Inhibitory Synaptic Transmission ◽  
Memory Traces ◽  
Brain Circuitry ◽  
Plastic Changes ◽  
Activity Dependent ◽  
The Brain

Abstract Activity-dependent plastic changes at synapses are essential for learning, but maintaining memory traces requires stable neuronal networks. The balance between plasticity and stability of the brain circuitry is tightly regulated. Among the mechanisms involved in regulating neuronal plasticity is the modulation of excitation and inhibition. Nogo-A was recently described for its ability to limit synaptic plasticity and to reciprocally regulate excitatory and inhibitory synaptic transmission.

scholarly journals Targeting Microglia-Synapse Interactions in Alzheimer’s Disease

2021 ◽  
Vol 22 (5) ◽  
pp. 2342
Author(s):  
Gaia Piccioni ◽  
Dalila Mango ◽  
Amira Saidi ◽  
Massimo Corbo ◽  
Robert Nisticò
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Intimate Relationship ◽  
Synapse Loss ◽  
Disease Modifying Therapy ◽  
Inflammatory Signals ◽  
Health And Disease ◽  
Activity Dependent ◽  
The Brain

In this review, we focus on the emerging roles of microglia in the brain, with particular attention to synaptic plasticity in health and disease. We present evidence that ramified microglia, classically believed to be “resting” (i.e., inactive), are instead strongly implicated in dynamic and plastic processes. Indeed, there is an intimate relationship between microglia and neurons at synapses which modulates activity-dependent functional and structural plasticity through the release of cytokines and growth factors. These roles are indispensable to brain development and cognitive function. Therefore, approaches aimed at maintaining the ramified state of microglia might be critical to ensure normal synaptic plasticity and cognition. On the other hand, inflammatory signals associated with Alzheimer’s disease are able to modify the ramified morphology of microglia, thus leading to synapse loss and dysfunction, as well as cognitive impairment. In this context, we highlight microglial TREM2 and CSF1R as emerging targets for disease-modifying therapy in Alzheimer’s disease (AD) and other neurodegenerative disorders.

scholarly journals Epigenetic Mechanisms in Memory and Cognitive Decline Associated with Aging and Alzheimer’s Disease

2021 ◽  
Vol 22 (22) ◽  
pp. 12280
Author(s):  
Sabyasachi Maity ◽  
Kayla Farrell ◽  
Shaghayegh Navabpour ◽  
Sareesh Naduvil Narayanan ◽  
Timothy J. Jarome
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Memory Loss ◽  
Memory Formation ◽  
Epigenetic Modifications ◽  
Epigenetic Mechanisms ◽  
Post Translational Modifications ◽  
Memory Decline ◽  
The Brain

Epigenetic mechanisms, which include DNA methylation, a variety of post-translational modifications of histone proteins (acetylation, phosphorylation, methylation, ubiquitination, sumoylation, serotonylation, dopaminylation), chromatin remodeling enzymes, and long non-coding RNAs, are robust regulators of activity-dependent changes in gene transcription. In the brain, many of these epigenetic modifications have been widely implicated in synaptic plasticity and memory formation. Dysregulation of epigenetic mechanisms has been reported in the aged brain and is associated with or contributes to memory decline across the lifespan. Furthermore, alterations in the epigenome have been reported in neurodegenerative disorders, including Alzheimer’s disease. Here, we review the diverse types of epigenetic modifications and their role in activity- and learning-dependent synaptic plasticity. We then discuss how these mechanisms become dysregulated across the lifespan and contribute to memory loss with age and in Alzheimer’s disease. Collectively, the evidence reviewed here strongly supports a role for diverse epigenetic mechanisms in memory formation, aging, and neurodegeneration in the brain.

scholarly journals MuSK Expressed in the Brain Mediates Cholinergic Responses, Synaptic Plasticity, and Memory Formation

2006 ◽  
Vol 26 (30) ◽  
pp. 7919-7932 ◽  
Author(s):  
A. Garcia-Osta ◽  
P. Tsokas ◽  
G. Pollonini ◽  
E. M. Landau ◽  
R. Blitzer ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Memory Formation ◽  
The Brain
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