scholarly journals Mg2+ Block of Drosophila NMDA Receptors Is Required for Long-Term Memory Formation and CREB-Dependent Gene Expression

Neuron ◽  
2012 ◽  
Vol 74 (5) ◽  
pp. 887-898 ◽  
Author(s):  
Tomoyuki Miyashita ◽  
Yoshiaki Oda ◽  
Junjiro Horiuchi ◽  
Jerry C.P. Yin ◽  
Takako Morimoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nmda Receptors ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Learning-induced gene expression in the heads of two Nasonia species that differ in long-term memory formation

BMC Genomics ◽  
2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Katja M Hoedjes ◽  
Hans M Smid ◽  
Elio GWM Schijlen ◽  
Louise EM Vet ◽  
Joke JFA van Vugt
Keyword(s):  
Gene Expression ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Dynamical Mechanisms for Gene Regulation Mediated by Two Noncoding RNAs in Long-Term Memory Formation

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Lijie Hao ◽  
Zhuoqin Yang
Keyword(s):  
Gene Expression ◽  
Gene Regulation ◽  
Regulation Of Gene Expression ◽  
Network Motif ◽  
Noncoding Rnas ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory ◽  
Motif Model

Noncoding RNAs such as miRNAs and piRNAs have long-lasting effects on the regulation of gene expression involved in long-term synaptic changes. To characterize gene regulation mediated by small noncoding RNAs associated with long-term memory in Aplysia, we consider two noncoding RNAs stimulated by 5-HT into a gene regulatory network motif model, including miR-124 that binds to and inhibits the mRNA of CREB1 and piR-F that facilitates serotonin-dependent DNA methylation to lead to repression of CREB2. Codimension-1 and -2 bifurcation analyses of 5-HT regulating both miR-124 and piR-F and a negative feedback strength for oscillation reveal rich dynamical properties of bistability and oscillations robust to variations in all other parameters. More importantly, we verify three stimulus protocols of 5-HT in experiments by our model and find that application of five pulses of 5-HT leads to a transient decrease of miR-124 but increase of piR-F concentrations, which matters sustained high level of CREB1 concentration associated with long-term memory. Furthermore, we perform bifurcation analyses for the concentrations of miR-124 and piR-F as two parameters to explore dynamical mechanisms underlying the epigenetic regulation in long-term memory formation. This study provides insights into revealing regulatory roles of epigenetic changes in gene expression involving noncoding RNAs associated with synaptic plasticity.

scholarly journals Transcription Factors in Long-Term Memory and Synaptic Plasticity

2009 ◽  
Vol 89 (1) ◽  
pp. 121-145 ◽  
Author(s):  
Cristina M. Alberini
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Synaptic Plasticity ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory ◽  
Molecular Neuroscience ◽  
And Function ◽  
Expression Evidence

Transcription is a molecular requisite for long-term synaptic plasticity and long-term memory formation. Thus, in the last several years, one main interest of molecular neuroscience has been the identification of families of transcription factors that are involved in both of these processes. Transcription is a highly regulated process that involves the combined interaction and function of chromatin and many other proteins, some of which are essential for the basal process of transcription, while others control the selective activation or repression of specific genes. These regulated interactions ultimately allow a sophisticated response to multiple environmental conditions, as well as control of spatial and temporal differences in gene expression. Evidence based on correlative changes in expression, genetic mutations, and targeted molecular inhibition of gene expression have shed light on the function of transcription in both synaptic plasticity and memory formation. This review provides a brief overview of experimental work showing that several families of transcription factors, including CREB, C/EBP, Egr, AP-1, and Rel, have essential functions in both processes. The results of this work suggest that patterns of transcription regulation represent the molecular signatures of long-term synaptic changes and memory formation.

scholarly journals Mushroom body-specific profiling of gene expression identifies regulators of long-term memory in Drosophila

2017 ◽  
Author(s):  
Yves F Widmer ◽  
Adem Bilican ◽  
Rémy Bruggmann ◽  
Simon G Sprecher
Keyword(s):  
Gene Expression ◽  
Learning And Memory ◽  
Mushroom Body ◽  
Memory Formation ◽  
Long Term Memory ◽  
Transcriptional Program ◽  
Term Memory ◽  
New Genes ◽  
Memory Traces

AbstractMemory formation is achieved by genetically tightly controlled molecular pathways that result in a change of synaptic strength and synapse organization. While for short-term memory traces rapidly acting biochemical pathways are in place, the formation of long-lasting memories requires changes in the transcriptional program of a cell. Although many genes involved in learning and memory formation have been identified, little is known about the genetic mechanisms required for changing the transcriptional program during different phases of long-term memory formation. With Drosophila melanogaster as a model system we profiled transcriptomic changes in the mushroom body, a memory center in the fly brain, at distinct time intervals during long-term memory formation using the targeted DamID technique. We describe the gene expression profiles during these phases and tested 33 selected candidate genes for deficits in long-term memory formation using RNAi knockdown. We identified 10 genes that enhance or decrease memory when knocked-down in the mushroom body. For vajk-1 and hacd1, the two strongest hits, we gained further support for their crucial role in learning and forgetting. These findings show that profiling gene expression changes in specific cell-types harboring memory traces provides a powerful entry point to identify new genes involved in learning and memory. The presented transcriptomic data may further be used as resource to study genes acting at different memory phases.

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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