scholarly journals Dnmts and Tet target memory-associated genes after appetitive olfactory training in honey bees

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Stephanie D. Biergans ◽  
C. Giovanni Galizia ◽  
Judith Reinhard ◽  
Charles Claudianos
Keyword(s):  
Dna Methylation ◽  
Honey Bees ◽  
Dna Methyltransferase ◽  
Time Course ◽  
Methylation Pattern ◽  
Memory Formation ◽  
Long Term Memory ◽  
Memory Retention ◽  
Term Memory

Abstract DNA methylation and demethylation are epigenetic mechanisms involved in memory formation. In honey bees DNA methyltransferase (Dnmt) function is necessary for long-term memory to be stimulus specific (i.e. to reduce generalization). So far, however, it remains elusive which genes are targeted and what the time-course of DNA methylation is during memory formation. Here, we analyse how DNA methylation affects memory retention, gene expression and differential methylation in stimulus-specific olfactory long-term memory formation. Out of 30 memory-associated genes investigated here, 9 were upregulated following Dnmt inhibition in trained bees. These included Dnmt3 suggesting a negative feedback loop for DNA methylation. Within these genes also the DNA methylation pattern changed during the first 24 hours after training. Interestingly, this was accompanied by sequential activation of the DNA methylation machinery (i.e. Dnmts and Tet). In sum, memory formation involves a temporally complex epigenetic regulation of memory-associated genes that facilitates stimulus specific long-term memory in the honey bee.

Dopamine interferes with appetitive long-term memory formation in honey bees

2013 ◽  
Vol 106 ◽  
pp. 230-237 ◽  
Author(s):  
Martín Klappenbach ◽  
Laura Kaczer ◽  
Fernando Locatelli
Keyword(s):  
Honey Bees ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Tet2 negatively regulates memory fidelity

2019 ◽  
Author(s):  
Kristine E. Zengeler ◽  
Caroline P. Gettens ◽  
Hannah C. Smith ◽  
Mallory M. Caron ◽  
Xinyuan Zhang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bisulfite Sequencing ◽  
Memory Formation ◽  
Negative Regulator ◽  
Long Term Memory ◽  
Term Memory ◽  
Glutamatergic Neurons ◽  
Genome Bisulfite Sequencing ◽  
Tet Enzymes

SummaryDespite being fully differentiated, DNA methylation is dynamically regulated in post-mitotic glutamatergic neurons in the CA1 of the hippocampus through competing active DNA methylation and de-methylation, a process that regulates neuronal plasticity. Active DNA methylation after learning is necessary for long-term memory formation, and active DNA de-methylation by the TET enzymes has been implicated as a counter-regulator of that biochemical process. We demonstrate that Tet2 functions in the CA1 as a negative regulator of long-term memory, whereby its knockdown across the CA1 or haploinsufficiency in glutamatergic neurons enhances the fidelity of hippocampal-dependent spatial and associative memory. Loci of altered DNA methylation were then determined using whole genome bisulfite sequencing from glutamatergic Tet2 haploinsufficient CA1 tissue, which revealed hypermethylation in the promoters of genes known to be transcriptionally regulated after experiential learning. This study demonstrates a link between Tet2 activity at genes important for memory formation in CA1 glutamatergic neurons and memory fidelity.

scholarly journals Role of protein synthesis and DNA methylation in the consolidation and maintenance of long-term memory in Aplysia

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Kaycey Pearce ◽  
Diancai Cai ◽  
Adam C Roberts ◽  
David L Glanzman
Keyword(s):  
Dna Methylation ◽  
Protein Synthesis ◽  
Dna Methyltransferase ◽  
Long Term Memory ◽  
Protein Synthesis Inhibition ◽  
Term Memory ◽  
Normal Expression ◽  
Later Phase

Previously, we reported that long-term memory (LTM) in Aplysia can be reinstated by truncated (partial) training following its disruption by reconsolidation blockade and inhibition of PKM (Chen et al., 2014). Here, we report that LTM can be induced by partial training after disruption of original consolidation by protein synthesis inhibition (PSI) begun shortly after training. But when PSI occurs during training, partial training cannot subsequently establish LTM. Furthermore, we find that inhibition of DNA methyltransferase (DNMT), whether during training or shortly afterwards, blocks consolidation of LTM and prevents its subsequent induction by truncated training; moreover, later inhibition of DNMT eliminates consolidated LTM. Thus, the consolidation of LTM depends on two functionally distinct phases of protein synthesis: an early phase that appears to prime LTM; and a later phase whose successful completion is necessary for the normal expression of LTM. Both the consolidation and maintenance of LTM depend on DNA methylation.

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.

scholarly journals Wnt Signaling Is Required for Long-Term Memory Formation

Cell Reports ◽  
2013 ◽  
Vol 4 (6) ◽  
pp. 1082-1089 ◽  
Author(s):  
Ying Tan ◽  
Dinghui Yu ◽  
Germain U. Busto ◽  
Curtis Wilson ◽  
Ronald L. Davis
Keyword(s):  
Wnt Signaling ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory

scholarly journals What's hot: the enhancing effects of thermal stress on long-term memory formation in Lymnaea stagnalis

2012 ◽  
Vol 215 (24) ◽  
pp. 4322-4329 ◽  
Author(s):  
M. L. Teskey ◽  
K. S. Lukowiak ◽  
H. Riaz ◽  
S. Dalesman ◽  
K. Lukowiak
Keyword(s):  
Thermal Stress ◽  
Lymnaea Stagnalis ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory
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