Astrocyte-Neuron Lactate Transport Is Required for Long-Term Memory Formation

Cell, Journal Year: 2011, Volume and Issue: 144(5), P. 810 - 823

Published: March 1, 2011

Language: Английский

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Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice

Nature Medicine, Journal Year: 2014, Volume and Issue: 20(6), P. 659 - 663

Published: May 4, 2014

Language: Английский

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Molecular Mechanisms of Fear Learning and Memory

Cell, Journal Year: 2011, Volume and Issue: 147(3), P. 509 - 524

Published: Oct. 1, 2011

Language: Английский

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

Philosophical Transactions of the Royal Society B Biological Sciences, Journal Year: 2013, Volume and Issue: 369(1633), P. 20130288 - 20130288

Published: Dec. 3, 2013

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

Language: Английский

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Histone Methylation Regulates Memory Formation

Journal of Neuroscience, Journal Year: 2010, Volume and Issue: 30(10), P. 3589 - 3599

Published: March 10, 2010

It has been established that regulation of chromatin structure through post-translational modification histone proteins, primarily H3 phosphorylation and acetylation, is an important early step in the induction synaptic plasticity formation long-term memory. In this study, we investigated contribution another modification, methylation, to memory adult hippocampus. We found trimethylation at lysine 4 (H3K4), active mark for transcription, upregulated hippocampus 1 h following contextual fear conditioning. addition, dimethylation 9 (H3K9), a molecular associated with transcriptional silencing, increased after conditioning decreased 24 context exposure alone Trimethylated H3K4 levels returned baseline h. also mice deficient H3K4-specific methyltransferase, Mll , displayed deficits relative wild-type animals. This suggests methylation required proper consolidation memories. Interestingly, inhibition deacetylases (HDACs) sodium butyrate (NaB) resulted H3K9 Correspondingly, learning triggered increases specific gene promoter regions ( Zif268 bdnf ) altered DNA MeCP2 binding. Together, these data demonstrate actively regulated facilitates formation.

Language: Английский

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HDAC3 Is a Critical Negative Regulator of Long-Term Memory Formation

Journal of Neuroscience, Journal Year: 2011, Volume and Issue: 31(2), P. 764 - 774

Published: Jan. 12, 2011

Gene expression is dynamically regulated by chromatin modifications on histone tails, such as acetylation. In general, acetylation promotes transcription, whereas deacetylation negatively regulates transcription. The interplay between acetyltranserases and deacetylases (HDACs) pivotal for the regulation of gene required long-term memory processes. Currently, very little known about role individual HDACs in learning memory. We examined HDAC3 using a combined genetic pharmacologic approach. used HDAC3–FLOX genetically modified mice combination with adeno-associated virus-expressing Cre recombinase to generate focal homozygous deletions Hdac3 area CA1 dorsal hippocampus. To complement this approach, we also selective inhibitor HDAC3, RGFP136 [ N -(6-(2-amino-4-fluorophenylamino)-6-oxohexyl)-4-methylbenzamide]. Immunohistochemistry showed that deletion or intrahippocampal delivery resulted increased Both well inhibition via significantly enhanced persistent manner. Next genes implicated from hippocampal punches quantitative reverse transcription-PCR. Expression nuclear receptor subfamily 4 group A, member 2 ( Nr4a2 ) c-fos was hippocampus compared wild-type controls. Memory enhancements observed were abolished small interfering RNA, suggesting mechanism which formation. Together, these findings demonstrate critical molecular mechanisms underlying

Language: Английский

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Tet1 Is Critical for Neuronal Activity-Regulated Gene Expression and Memory Extinction

Neuron, Journal Year: 2013, Volume and Issue: 79(6), P. 1109 - 1122

Published: Sept. 1, 2013

Language: Английский

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Lactate promotes plasticity gene expression by potentiating NMDA signaling in neurons

Proceedings of the National Academy of Sciences, Journal Year: 2014, Volume and Issue: 111(33), P. 12228 - 12233

Published: July 28, 2014

Significance The transfer of lactate, a product aerobic glycolysis, from astrocytes to neurons was recently shown be necessary for the establishment long-term memory and maintenance in vivo potentiation. Here, we report that lactate induces expression plasticity genes such as Arc, c-Fos, Zif268 neurons. action is mediated by modulation NMDA receptor activity downstream Erk1/2 signaling cascade, through mechanism associated with changes cellular redox state. These observations unveil an unexpected role molecule addition its energy metabolism open previously unidentified research avenue study neuronal memory.

Language: Английский

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CREB's control of intrinsic and synaptic plasticity: implications for CREB-dependent memory models

Trends in Neurosciences, Journal Year: 2010, Volume and Issue: 33(5), P. 230 - 240

Published: March 11, 2010

Language: Английский

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A critical role for IGF-II in memory consolidation and enhancement

Nature, Journal Year: 2011, Volume and Issue: 469(7331), P. 491 - 497

Published: Jan. 1, 2011

Language: Английский

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