Epigenetic codes in cognition and behaviour.

doi:10.1016/J.BBR.2008.01.021

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Epigenetic codes in cognition and behaviour.

Journal Article•DOI•

Epigenetic codes in cognition and behaviour.

Johannes Gräff¹, Isabelle M. Mansuy¹•Institutions (1)

École Polytechnique Fédérale de Lausanne¹

01 Sep 2008-Behavioural Brain Research (Elsevier)-Vol. 192, Iss: 1, pp 70-87

TL;DR: Recent findings on the role and mechanisms of epigenetic codes in the brain are described, and their implication in synaptic plasticity, cognitive functions and psychiatric disorders are discussed.

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About: This article is published in Behavioural Brain Research.The article was published on 2008-09-01. It has received 260 citations till now. The article focuses on the topics: Epigenetic code & Epigenetics.

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Journal Article•DOI•

Socioeconomic status and the developing brain

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Daniel A. Hackman¹, Martha J. Farah¹•Institutions (1)

University of Pennsylvania¹

01 Feb 2009-Trends in Cognitive Sciences

TL;DR: These studies indicate that SES is an important predictor of neurocognitive performance, particularly of language and executive function, and that S ES differences are found in neural processing even when performance levels are equal.

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1,258 citations

Journal Article•DOI•

Lasting epigenetic influence of early-life adversity on the BDNF gene.

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Tania L. Roth¹, Farah D. Lubin¹, Adam J. Funk¹, J. David Sweatt¹•Institutions (1)

University of Alabama at Birmingham¹

01 May 2009-Biological Psychiatry

TL;DR: An epigenetic molecular mechanism potentially underlying lifelong and transgenerational perpetuation of changes in gene expression and behavior incited by early abuse and neglect is highlighted.

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1,176 citations

Journal Article•DOI•

Transcription Factors in Long-Term Memory and Synaptic Plasticity

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Cristina M. Alberini¹•Institutions (1)

Icahn School of Medicine at Mount Sinai¹

01 Jan 2009-Physiological Reviews

TL;DR: The results of this work suggest that patterns of transcription regulation represent the molecular signatures of long-term synaptic changes and memory formation.

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Abstract: 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 ...

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902 citations

Cites background from "Epigenetic codes in cognition and b..."

...[From Gräff and Mansuy (82), with permission from Elsevier....
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...[From Gräff and Mansuy (82), with permission from Elsevier.]...
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Journal Article•DOI•

Histone acetylation: molecular mnemonics on the chromatin

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Johannes Gräff¹, Li-Huei Tsai², Li-Huei Tsai¹•Institutions (2)

Massachusetts Institute of Technology¹, Picower Institute for Learning and Memory²

01 Feb 2013-Nature Reviews Neuroscience

TL;DR: As histone acetylation and cognitive functions can be pharmacologically restored by histone deacetylase inhibitors, this epigenetic modification might constitute a molecular memory aid on the chromatin and, by extension, a new template for therapeutic interventions against cognitive frailty.

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Abstract: Long-lasting memories require specific gene expression programmes that are, in part, orchestrated by epigenetic mechanisms. Of the epigenetic modifications identified in cognitive processes, histone acetylation has spurred considerable interest. Whereas increments in histone acetylation have consistently been shown to favour learning and memory, a lack thereof has been causally implicated in cognitive impairments in neurodevelopmental disorders, neurodegeneration and ageing. As histone acetylation and cognitive functions can be pharmacologically restored by histone deacetylase inhibitors, this epigenetic modification might constitute a molecular memory aid on the chromatin and, by extension, a new template for therapeutic interventions against cognitive frailty.

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506 citations

Journal Article•DOI•

Finding the engram.

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Sheena A. Josselyn, Stefan Köhler¹, Paul W. Frankland•Institutions (1)

University of Western Ontario¹

01 Sep 2015-Nature Reviews Neuroscience

TL;DR: This Review develops four defining criteria that enable us to critically assess the recent progress that has been made towards finding the engram, and proposes that findings from 'capture' studies represent considerable progress in allowing us to observe, erase and express the engrams.

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Abstract: Many attempts have been made to localize the physical trace of a memory, or engram, in the brain However, until recently, engrams have remained largely elusive In this Review, we develop four defining criteria that enable us to critically assess the recent progress that has been made towards finding the engram Recent 'capture' studies use novel approaches to tag populations of neurons that are active during memory encoding, thereby allowing these engram-associated neurons to be manipulated at later times We propose that findings from these capture studies represent considerable progress in allowing us to observe, erase and express the engram

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464 citations

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References

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Journal Article•DOI•

Evidence That DNA (Cytosine-5) Methyltransferase Regulates Synaptic Plasticity in the Hippocampus

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Jonathan M. Levenson¹, Tania L. Roth¹, Farah D. Lubin¹, Courtney A. Miller¹, I-Chia Huang¹, Priyanka Desai¹, Lauren M. Malone¹, J. David Sweatt¹ - Show less +4 more•Institutions (1)

Baylor College of Medicine¹

09 Jun 2006-Journal of Biological Chemistry

TL;DR: In this article, the role of DNA methyltransferase (DNMT) activity in regulating the induction of synaptic plasticity was examined and it was found that the DNA within promoters for reelin and brain-derived neurotrophic factor exhibited rapid and dramatic changes in cytosine methylation when DNMT activity was inhibited.

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589 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...Blockade of DNA ethylation by DNMT inhibitors such as zebularine or 5-aza-deoxycytidine (5-aza) impairs the induction of LTP in the ippocampus [42]....
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...[42] Levenson JM, Roth TL, Lubin FD, Miller CA, Huang IC, Desai P, et...
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...DNA methylation is another epigenetic mechanism that conributes to regulate synaptic plasticity [42]....
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...ces LTP Hippocampus Mice [43] ctivity blocks LTP Hippocampus Mice [42]...
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...In ontrast, BDNF expression is significantly upregulated and H4 yperacetylated at BDNF promoter P2 by pilocarpine treatment. lectroconvulsive seizures (ECS) also modulate H4 acetylation n the promoter region of c-Fos, BDNF and CREB genes, and corelate with altered mRNA expression in that H4 hyperacetylation s associated with increased gene expression and vice versa [45]. owever, there is no clear correlation for H3 acetylation on K9 or 14, or for the combined phosphorylation/acetylation of Ser10 nd K14, suggesting a general role for H4 acetylation but a more Brain area Organism References ces LTP Hippocampus Mice [43] ctivity blocks LTP Hippocampus Mice [42] irs spatial memory Hippocampus Mice [43] 1, a memory eased while memory promoting ntext learning Hippocampus Rats [48] 4K8 acetylation on AT CBP Sensory-motor neurons Aplysia [29] ion is accompanied tion Hippocampus Rats [36] X repressor group of y is accompanied by Hippocampus Mice [38] in H2B e-phase LTP Hippocampus Mice [39] Bdnf, H4 R2 observed in acute cetylation only in Hippocampus Rats [44,45] APK is regulating in novel taste Insular cortex Mice [49] loinsufficiency Hippocampus and forebrain Mice [39,50] spatial memory Hippocampus Mice [51] creased by spatial Hippocampus Rats [36] Bdnf promoters is d fear Prefrontal cortex Mice [55] is regulated by the nd increased upon ning Hippocampus Rats [53] g protein; C/EBP, CCAAT/enhancer binding protein; DNMT1, DNA methyl HAT, histone acetyl transferase; LTF, long-term facilitation; LTP, long-term protein 1; NMDA, N-methyl d-aspartate; PP1, protein phosphatase 1....
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Journal Article•DOI•

Mild overexpression of MeCP2 causes a progressive neurological disorder in mice

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Ann L. Collins¹, Jonathan M. Levenson, Alexander P. Vilaythong, Ronald Richman, Dawna L. Armstrong, Jeffrey L. Noebels, J. David Sweatt, Huda Y. Zoghbi - Show less +4 more•Institutions (1)

Baylor College of Medicine¹

01 Nov 2004-Human Molecular Genetics

TL;DR: The data demonstrate that MeCP2 levels must be tightly regulated in vivo, and that even mild overexpression of this protein is detrimental, and support the possibility that duplications or gain-of-function mutations in MECP2 might underlie some cases of X-linked delayed-onset neurobehavioral disorders.

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Abstract: Mutations in the X-linked methyl-CpG-binding protein 2 (MECP2), encoding a transcriptional repressor, cause Rett syndrome and a variety of related neurodevelopmental disorders. The vast majority of mutations associated with human disease are loss-of-function mutations, but precisely what aspect of MeCP2 function is responsible for these phenotypes remains unknown. We overexpressed wild-type human protein in transgenic mice using a large genomic clone containing the entire human MECP2 locus. Detailed neurobehavioral and electrophysiological studies in transgenic line MeCP2(Tg1), which expresses MeCP2 at approximately 2-fold wild-type levels, demonstrated onset of phenotypes around 10 weeks of age. Surprisingly, these mice displayed enhanced motor and contextual learning and enhanced synaptic plasticity in the hippocampus. After 20 weeks of age, however, these mice developed seizures, became hypoactive and approximately 30% of them died by 1 year of age. These data demonstrate that MeCP2 levels must be tightly regulated in vivo, and that even mild overexpression of this protein is detrimental. Furthermore, these results support the possibility that duplications or gain-of-function mutations in MECP2 might underlie some cases of X-linked delayed-onset neurobehavioral disorders.

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574 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...[65] Collins AL, Levenson JM, Vilaythong AP, Richman R, Armstrong DL,...
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...MeCP2 deficiency increases nxiety, and a two-fold overexpression of human MeCP2 in ice carrying a truncated endogenous form of MeCP2 was hown to enhance synaptic plasticity in the hippocampus and to mprove spatial memory [65]....
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Journal Article•DOI•

Heightened synaptic plasticity of hippocampal CA1 neurons during a cholinergically induced rhythmic state.

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Patriclo T. Huerta¹, John E. Lisman¹•Institutions (1)

Brandeis University¹

19 Aug 1993-Nature

TL;DR: The results suggest that cholinergic systems may affect memory formation through the induction of an oscillatory state in which the requirements for synaptic plasticity are dramatically altered.

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Abstract: Brain cholinergic neurons are critical for memory function and their loss may contribute to memory impairment in Alzheimer's disease One role of cholinergic neurons is to elicit an oscillatory activity called theta rhythm in the hippocampus, a brain region involved in memory processing Theta rhythm occurs during periods of learning, but its effect on the synaptic plasticity that underlies learning remains unclear We have studied synaptic plasticity in hippocampal slices during theta-frequency oscillations induced by a cholinergic agonist Here we report that during these oscillations, synapses are in a state of heightened plasticity and can be modified by what would otherwise be ineffective stimulation This heightened plasticity is sensitive to the timing of incoming stimuli with respect to the oscillatory activity The results suggest that cholinergic systems may affect memory formation through the induction of an oscillatory state in which the requirements for synaptic plasticity are dramatically altered

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570 citations

Journal Article•DOI•

Special HATs for special occasions: linking histone acetylation to chromatin assembly and gene activation

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J. E. Brownell¹, C. David Allis¹•Institutions (1)

University of Rochester¹

01 Apr 1996-Current Opinion in Genetics & Development

TL;DR: Ongoing characterization of these enzymes and their molecular cohorts supports a direct role for acetylation in a signaling pathway that modulates chromatin structure to create new patterns of transcription.

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550 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...It esults in the neutralization of the positive charge of the -amino roup of lysine (K) residues in the histone tail, which decreases he affinity between the protein tail and the DNA, and relaxes he chromatin structure [13]....
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Journal Article•DOI•

Time-Dependent Increases in Brain-Derived Neurotrophic Factor Protein Levels within the Mesolimbic Dopamine System after Withdrawal from Cocaine: Implications for Incubation of Cocaine Craving

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Jeffrey W. Grimm¹, Lin Lu, Teruo Hayashi¹, Bruce T. Hope, Tsung-Ping Su¹, Yavin Shaham - Show less +2 more•Institutions (1)

National Institute on Drug Abuse¹

01 Feb 2003-The Journal of Neuroscience

TL;DR: Time-dependent increases in BDNF levels may lead to synaptic modifications that underlie enhanced responsiveness to cocaine cues after prolonged withdrawal periods, and these changes were observed during tests for sucrose craving.

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Abstract: Using a rat model of drug craving, we found that the responsiveness to cocaine cues progressively increases or incubates over the first 60 d of cocaine withdrawal. Here we studied whether alterations in brain-derived neurotrophic factor (BDNF) protein levels within the mesolimbic dopamine system are associated with this incubation phenomenon. BDNF is involved in synaptic plasticity and was found to enhance responding for cues associated with natural rewards. Rats were trained to press a lever to receive intravenous cocaine or oral sucrose for 6 hr/d for 10 d; each earned reward was paired with a tone–light cue. Resumption of lever-pressing behavior was then assessed on days 1, 30, or 90 of reward withdrawal. First, resistance to extinction was assessed during 6 hr in which lever presses were not reinforced and the cue was absent. Second, cue-induced reinstatement was assessed after extinction during 1 hr in which responding led to cue presentations. Other rats were killed without testing on days 1, 30, and 90 of reward withdrawal, and BDNF and nerve growth factor (NGF) protein levels were measured in the ventral tegmental area (VTA), accumbens, and amygdala. Lever pressing during extinction and cue-induced reinstatement tests of cocaine craving progressively increased after cocaine withdrawal. Time-dependent changes also were observed during the tests for sucrose craving, with maximal responding on day 30. BDNF, but not NGF, levels in the VTA, accumbens, and amygdala progressively increased after cocaine, but not sucrose, withdrawal. Time-dependent increases in BDNF levels may lead to synaptic modifications that underlie enhanced responsiveness to cocaine cues after prolonged withdrawal periods.

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543 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...[97] Grimm JW, Lu L, Hayashi T, Hope BT, Su TP, Shaham Y....
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...hronic cocaine treatment by self-administration also leads to 3 hyperacetylation in the promoter region of FosB, as well as f Bdnf and Cdk5 [94], which are activated by chronic cocaine xposure in the striatum [97,98]....
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