Decreased level of histone acetylation in the infralimbic prefrontal cortex following immediate extinction may result in deficit of extinction memory

Singh, Sanjay; Siddiqui, Sarfraj Ahmad; Tripathy, Sukanya; Kumar, Shailendra; Saha, Sudipta; Ugale, Rajesh R.; Modi, Dinesh Raj; Prakash, Anand

doi:10.1016/j.brainresbull.2018.06.004

Cited by 12 publications

(10 citation statements)

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“…Indeed, the immediate extinction deficit emerged, which was however restricted to the stimulus not subject to a contextual change during extinction (stimulus c). Thus, our current findings are in large agreement with, but also extend beyond previous literature on the immediate extinction deficit in rodents (Maren and Chang 2006;Woods and Bouton 2008;Maren 2009, 2011;Chang et al 2010;Kim et al 2010;MacPherson et al 2013;Stafford et al 2013;Hollis et al 2016;Giustino et al 2017;Singh et al 2018; but see Myers et al 2006) and humans (Alvarez et al 2007;Schiller et al 2008;Huff et al 2009;Merz et al 2016; but see Norrholm et al 2008;Golkar and Öhman 2012).…”

Section: Discussionsupporting

confidence: 92%

“…The contextual change during extinction might serve as a strong cue that a new association might be established in contrast to a situation with no contextual change. In addition to the critical role of the infralimbic cortex (Chang et al 2010;Kim et al 2010;Singh et al 2018) and the basolateral amygdala (Giustino et al 2017) for the immediate extinction deficit, contextual processing of critical stimuli in the hippocampus (Maren et al 2013) could thus represent a reasonable mechanism for the reported differential effects to be characterized in future efforts. Similarly, the interrelationship between stimuli and contexts could be explored further to gain more insights into the underlying mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Time-dependent changes of extinction processes have been described in the immediate extinction deficit: extinguished responses recover more easily and stronger when extinction immediately follows acquisition in contrast to extinction taking place after a delay (delayed extinction; usually 24 h after acquisition; Maren 2014). This deficit has been shown in particular using fear conditioning paradigms in rodents (Maren and Chang 2006;Woods and Bouton 2008;Maren 2009, 2011;Chang et al 2010;Kim et al 2010;MacPherson et al 2013;Stafford et al 2013;Hollis et al 2016;Giustino et al 2017;Singh et al 2018; but see Myers et al 2006) and humans (Alvarez et al 2007;Schiller et al 2008;Huff et al 2009;Merz et al 2016; but see Norrholm et al 2008;Golkar and Öhman 2012). Presumably, emotional and stress responses evoked by the fear acquisition procedure (due to the accompanying application of aversive shocks) are still present during subsequent immediate extinction, but not during delayed extinction.…”

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confidence: 96%

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The immediate extinction deficit occurs in a nonemotional learning paradigm

Merz

Wolf

2019

Learn. Mem.

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The immediate extinction deficit describes a higher return of fear when extinction takes place immediately after fear acquisition compared to a delayed extinction design. One explanation for this phenomenon encompasses the remaining emotional arousal evoked by fear acquisition to be still present during immediate, but not delayed extinction. In the present study, the predictive learning task, a learning task not involving arousal or stress, was used testing the hypothesis that no immediate extinction deficit should occur in this neutral task. Twenty-six participants underwent an immediate extinction procedure and were tested in a recall session 24 h later. For the delayed extinction group (n = 26), acquisition, extinction, and recall were realized 24 h apart from each other. Recall performance of a third group (n = 26) was tested 48 h after the immediate extinction procedure. The immediate extinction deficit was indeed observed for a stimulus not subject to a contextual change from acquisition to extinction, but not for other stimuli involving contextual changes or no extinction control stimuli. Even in a neutral learning task and without emotional arousal, the immediate extinction deficit could be detected but was restricted to the specific contextual embedding of stimuli. Thus, contextual processing appears to differentially modulate the emergence of the immediate extinction deficit.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

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The immediate extinction deficit occurs in a nonemotional learning paradigm

Merz

Wolf

2019

Learn. Mem.

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“…Hypermethylation of Nr3c1 gene [26] Rat amygdala Hypermethylation of developing brain [27] Rat amygdala BDNF gene hypermethylation [28] Rat amygdala Aberrant HDAC2-mediated histone modifications [29] Rat hippocampus Differential histone acetylation and methylation [30] Rat hippocampus H3 histone acetylation; modulation of methyl-CpG-binding [31] Mouse cerebral cortex Down-regulation of HDAC2 associated with BDNF gene [32] Rat hippocampus Reduces H3K14 acetylation due to prenatal dexamethasone [33] Rat hippocampus Decreases H3K9 and H4K12 acetylation due to social isolation [34] Rat PFC Reduces H3/H4 acetylation after extinction training [35] Rat nucleus accumbens Inhibition of G9a/GLP HMT [36] Mouse medulla oblongata Histone modifications of genes affecting neurodevelopment and emotionality [37] Mouse hippocampus and amygdala Dysregulation of miR-132/212 [38] Rat amygdala Over-expression of miR-101a and its target Ezh2 [39] Rat PFC and hippocampus Changes in miRNA-135a and miRNA-16 [40] Rat amygdala and PFC Microbial regulation of miRNA expression [41] Mouse PFC lncRNA Gomafu associated with anxiety [42] GABA than healthy controls. 43,44 However, the data on GABA concentrations in plasma and cerebrospinal fluid of patients with anxiety is contradictory, possibly due to differences between studies in study design and methodology, tissues where sampling was done, and patient populations.…”

Section: Rat Hippocampusmentioning

confidence: 99%

<p>The Potential Role of Epigenetic Drugs in the Treatment of Anxiety Disorders</p>

Peedicayil¹

2020

NDT

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There is increasing evidence that abnormalities in epigenetic mechanisms of gene expression contribute to the pathogenesis of anxiety disorders (ADs). This article discusses the role of epigenetic mechanisms of gene expression in the pathogenesis of ADs. It also discusses the data so far obtained from preclinical and clinical trials on the use of epigenetic drugs for treating ADs. Most drug trials investigating the use of epigenetic drugs for treating ADs have used histone deacetylase inhibitors (HDACi). HDACi are showing favorable results in both preclinical and clinical drug trials for treating ADs. However, at present the mode of action of HDACi in ADs is not clear. More work needs to be done to elucidate how epigenetic dysregulation contributes to the pathogenesis of ADs. More work also needs to be done on the mode of action of HDACi in alleviating the signs and symptoms of ADs.

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“…There was differential H4K5ac in prefrontal cortex, significantly decreasing in infralimbic-prefrontal cortex (IL-PFC) and increasing in PL-PFC after fear learning. Histone acetylation also differed after fear extinction [44], with rat IL-PFC H3K9ac significantly higher after delayed extinction than after no or immediate extinction.…”

Section: Overview Of Epigenetic Markers In Ptsdmentioning

confidence: 99%

A Review of Epigenetics of PTSD in Comorbid Psychiatric Conditions

Blacker

Frye

Morava

et al. 2019

Genes

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Post-traumatic stress disorder (PTSD) is an acquired psychiatric disorder with functionally impairing physiological and psychological symptoms following a traumatic exposure. Genetic, epigenetic, and environmental factors act together to determine both an individual’s susceptibility to PTSD and its clinical phenotype. In this literature review, we briefly review the candidate genes that have been implicated in the development and severity of the PTSD phenotype. We discuss the importance of the epigenetic regulation of these candidate genes. We review the general epigenetic mechanisms that are currently understood, with examples of each in the PTSD phenotype. Our focus then turns to studies that have examined PTSD in the context of comorbid psychiatric disorders or associated social and behavioral stressors. We examine the epigenetic variation in cases or models of PTSD with comorbid depressive disorders, anxiety disorders, psychotic disorders, and substance use disorders. We reviewed the literature that has explored epigenetic regulation in PTSD in adverse childhood experiences and suicide phenotypes. Finally, we review some of the information available from studies of the transgenerational transmission of epigenetic variation in maternal cases of PTSD. We discuss areas pertinent for future study to further elucidate the complex interactions between epigenetic modifications and this complex psychiatric disorder.

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Decreased level of histone acetylation in the infralimbic prefrontal cortex following immediate extinction may result in deficit of extinction memory

Cited by 12 publications

References 78 publications

The immediate extinction deficit occurs in a nonemotional learning paradigm

The immediate extinction deficit occurs in a nonemotional learning paradigm

<p>The Potential Role of Epigenetic Drugs in the Treatment of Anxiety Disorders</p>

A Review of Epigenetics of PTSD in Comorbid Psychiatric Conditions

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