scholarly journals Sensory Cortical Plasticity Participates in the Epigenetic Regulation of Robust Memory Formation

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Mimi L. Phan ◽  
Kasia M. Bieszczad
Keyword(s):  
Epigenetic Regulation ◽  
Neural Plasticity ◽  
Cortical Plasticity ◽  
Memory Formation ◽  
Sensory Cortex ◽  
Long Term Memory ◽  
Epigenetic Mechanisms ◽  
Significant Information ◽  
Expression Of Genes ◽  
Open Question

Neuroplasticity remodels sensory cortex across the lifespan. A function of adult sensory cortical plasticity may be capturing available information during perception for memory formation. The degree of experience-dependent remodeling in sensory cortex appears to determine memory strength and specificity for important sensory signals. A key open question is how plasticity is engaged to induce different degrees of sensory cortical remodeling. Neural plasticity for long-term memory requires the expression of genes underlying stable changes in neuronal function, structure, connectivity, and, ultimately, behavior. Lasting changes in transcriptional activity may depend on epigenetic mechanisms; some of the best studied in behavioral neuroscience are DNA methylation and histone acetylation and deacetylation, which, respectively, promote and repress gene expression. One purpose of this review is to propose epigenetic regulation of sensory cortical remodeling as a mechanism enabling the transformation of significant information from experiences into content-rich memories of those experiences. Recent evidence suggests how epigenetic mechanisms regulate highly specific reorganization of sensory cortical representations that establish a widespread network for memory. Thus, epigenetic mechanisms could initiate events to establish exceptionally persistent and robust memories at a systems-wide level by engaging sensory cortical plasticity for gatingwhatandhow muchinformation becomes encoded.

Rapid Cortical Plasticity Supports Long-Term Memory Formation

2019 ◽  
Vol 23 (12) ◽  
pp. 989-1002 ◽  
Author(s):  
Melissa Hebscher ◽  
Erik Wing ◽  
Jennifer Ryan ◽  
Asaf Gilboa
Keyword(s):  
Cortical Plasticity ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Kynurenine, 3-OH-kynurenine, and anthranilate are nutrient metabolites that alter H3K4 trimethylation and H2AS40 O-GlcNAcylation at hypothalamus-related loci

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Koji Hayakawa ◽  
Kenta Nishitani ◽  
Satoshi Tanaka
Keyword(s):  
Gene Expression ◽  
Epigenetic Regulation ◽  
Epigenetic Modification ◽  
Neural Cells ◽  
Epigenetic Mechanisms ◽  
Post Translational Modifications ◽  
H3k4 Trimethylation ◽  
Expression Of Genes ◽  
Nutritional Conditions ◽  
Hypothalamic Function

AbstractEpigenetic mechanisms can establish and maintain mitotically stable patterns of gene expression while retaining the DNA sequence. These mechanisms can be affected by environmental factors such as nutrients. The importance of intracellular dosages of nutrient metabolites such as acetyl coenzyme A and S-adenosylmethionine, which are utilized as donors for post-translational modifications, is well-known in epigenetic regulation; however, the significance of indirect metabolites in epigenetic regulation is not clear. In this study, we screened for metabolites that function as epigenetic modulators. Because the expression of genes related to hypothalamic function is reportedly affected by nutritional conditions, we used a neural cell culture system and evaluated hypothalamic-linked loci. We supplemented the culture medium with 129 metabolites separately during induction of human-iPS-derived neural cells and used high-throughput ChIP-qPCR to determine the epigenetic status at 37 hypothalamus-linked loci. We found three metabolites (kynurenine, 3-OH-kynurenine, and anthranilate) from tryptophan pathways that increased H3K4 trimethylation and H2AS40 O-GlcNAcylation, resulting in upregulated gene expression at most loci, except those encoding pan-neural markers. Dietary supplementation of these three metabolites and the resulting epigenetic modification were important for stability in gene expression. In conclusion, our findings provide a better understanding of how nutrients play a role in epigenetic mechanisms.

Epigenetic Mechanisms

2011 ◽  
Vol 17 (6) ◽  
pp. 616-632 ◽  
Author(s):  
Farah D. Lubin ◽  
Swati Gupta ◽  
R. Ryley Parrish ◽  
Nicola M. Grissom ◽  
Robin L. Davis
Keyword(s):  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Posttranslational Modifications ◽  
Brain Regions ◽  
Memory Formation ◽  
Memory Storage ◽  
Long Term Memory ◽  
Epigenetic Mechanisms ◽  
Transcription Factor Activation ◽  
And Behavior

Recent advances in chromatin biology have identified a role for epigenetic mechanisms in the regulation of neuronal gene expression changes, a necessary process for proper synaptic plasticity and memory formation. Experimental evidence for dynamic chromatin remodeling influencing gene transcription in postmitotic neurons grew from initial reports describing posttranslational modifications of histones, including phosphorylation and acetylation occurring in various brain regions during memory consolidation. An accumulation of recent studies, however, has also highlighted the importance of other epigenetic modifications, such as DNA methylation and histone methylation, as playing a role in memory formation. This present review examines learning-induced gene transcription by chromatin remodeling underlying long-lasting changes in neurons, with direct implications for the study of epigenetic mechanisms in long-term memory formation and behavior. Furthermore, the study of epigenetic gene regulation, in conjunction with transcription factor activation, can provide complementary lines of evidence to further understanding transcriptional mechanisms subserving memory storage.

scholarly journals Effect of PLL treatment on the long-term memory formation in Helix mollusk

2020 ◽  
Author(s):  
Larissa N. Grinkevich
Keyword(s):  
Mature Mirnas ◽  
Memory Formation ◽  
Mirna Biogenesis ◽  
Long Term Memory ◽  
Training Procedure ◽  
Epigenetic Mechanisms ◽  
Food Aversion ◽  
Significant Deterioration ◽  
Term Memory

Relevance. The studies of the epigenetic mechanisms of long-term memory formation (LTM) has attracted the attention of many world leading laboratories since gained knowledge can be applied to correct cognitive impairments. miRNA dependent suppression of gene expression is the most complicated step in the epigenetic regulation, associated with a huge number of miRNAs (tens of thousands) and the diversity of their targets, thus the knowledge of miRNAs functions during LTM is still very fragmented. Aim. The aim of this study was to investigate the involvement of miRNAs in the formation of long-term memory using the model of the food aversion conditioned reflex development in the mollusk Helix. Prevention of the formation of mature miRNAs via Poly-L-lysine hydrobromide (PLL) treatment - inhibitor of Dicer activity was used as the main approach. Materials and methods. PLL was injected into animals during training, or 1, 3 or 5 hours after training. Success of the formation of conditioned reflexes was tested 72 hours after training. Results. There was a significant deterioration in LTM in animals with injected PLL 1 and 3 hours after training procedure compared with trained animals that were not injected with PLL. The treatment with PLL during training, or 5 hours after training, had no effect on LTM. Conclusion. Treatment with PLL, inhibitor of miRNA biogenesis disrupts formation of the food aversion reflex in Helix. Thus, miNRAs are involved in the LTM formation on Helix. Impaired expression of miRNAs is critical for the long-term memory formation if occurs in the intervals of 1 to 3 hours after training. We can recommend PLL for the investigations in the area of the epigenetic mechanisms of long-term memory.

Adaptive and Maladaptive Neural Plasticity Due to Facial Nerve Palsy

2016 ◽  
Vol 224 (2) ◽  
pp. 102-111 ◽  
Author(s):  
Carsten M. Klingner ◽  
Stefan Brodoehl ◽  
Gerd F. Volk ◽  
Orlando Guntinas-Lichius ◽  
Otto W. Witte
Keyword(s):  
Facial Nerve ◽  
Neural Plasticity ◽  
Cortical Plasticity ◽  
Brain Plasticity ◽  
Motor Nerve ◽  
Predictive Coding ◽  
Theoretical Framework ◽  
Cortical Reorganization ◽  
Nerve Lesion ◽  
Peripheral Facial Palsy

Abstract. This paper reviews adaptive and maladaptive mechanisms of cortical plasticity in patients suffering from peripheral facial palsy. As the peripheral facial nerve is a pure motor nerve, a facial nerve lesion is causing an exclusive deefferentation without deafferentation. We focus on the question of how the investigation of pure deefferentation adds to our current understanding of brain plasticity which derives from studies on learning and studies on brain lesions. The importance of efference and afference as drivers for cortical plasticity is discussed in addition to the crossmodal influence of different competitive sensory inputs. We make the attempt to integrate the experimental findings of the effects of pure deefferentation within the theoretical framework of cortical responses and predictive coding. We show that the available experimental data can be explained within this theoretical framework which also clarifies the necessity for maladaptive plasticity. Finally, we propose rehabilitation approaches for directing cortical reorganization in the appropriate direction and highlight some challenging questions that are yet unexplored in the field.

scholarly journals Disruption of the astrocyte–neuron interaction is responsible for the impairments in learning and memory in 5XFAD mice: an Alzheimer’s disease animal model

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Moonseok Choi ◽  
Sang-Min Lee ◽  
Dongsoo Kim ◽  
Heh-In Im ◽  
Hye-Sun Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory ◽  
Stat3 Phosphorylation ◽  
Neuron Interactions ◽  
5Xfad Mice

AbstractThe morphological dynamics of astrocytes are altered in the hippocampus during memory induction. Astrocyte–neuron interactions on synapses are called tripartite synapses. These control the synaptic function in the central nervous system. Astrocytes are activated in a reactive state by STAT3 phosphorylation in 5XFAD mice, an Alzheimer’s disease (AD) animal model. However, changes in astrocyte–neuron interactions in reactive or resting-state astrocytes during memory induction remain to be defined. Here, we investigated the time-dependent changes in astrocyte morphology and the number of astrocyte–neuron interactions in the hippocampus over the course of long-term memory formation in 5XFAD mice. Hippocampal-dependent long-term memory was induced using a contextual fear conditioning test in 5XFAD mice. The number of astrocytic processes increased in both wild-type and 5XFAD mice during memory formation. To assess astrocyte–neuron interactions in the hippocampal dentate gyrus, we counted the colocalization of glial fibrillary acidic protein and postsynaptic density protein 95 via immunofluorescence. Both groups revealed an increase in astrocyte–neuron interactions after memory induction. At 24 h after memory formation, the number of tripartite synapses returned to baseline levels in both groups. However, the total number of astrocyte–neuron interactions was significantly decreased in 5XFAD mice. Administration of Stattic, a STAT3 phosphorylation inhibitor, rescued the number of astrocyte–neuron interactions in 5XFAD mice. In conclusion, we suggest that a decreased number of astrocyte–neuron interactions may underlie memory impairment in the early stages of AD.

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