Global epigenetic analysis of BDNF Val66Met mice hippocampus reveals changes in dendrite and spine remodeling genes

Mallei, Alessandra; Ieraci, Alessandro; Corna, Stefano; Tardito, Daniela; Lee, Francis S.; Popoli, Maurizio

doi:10.1002/hipo.22991

Cited by 14 publications

(9 citation statements)

References 88 publications

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“…For example, a rich literature indicates that repeated cocaine causes a prolonged accumulation of FosB and its isoforms in the NAcc (Nestler, 2004;Chandra and Lobo, 2017). FosB tran-scription is promoted by the activation of the D1 dopamine receptor-cAMP-PKA-CREB pathway and, among other things, FosB enhances the transcription of BDNF, which increases dendritic spine density (Zhang et al, 2002;Mallei et al, 2018). The current finding that the transcription factor Npas4, which is a target of HDAC5 (Taniguchi et al, 2017), is overexpressed in the NAcc of cocaine self-administering mice is consistent with a recent study demonstrating that experimenter-delivered cocaine increased Npas4 expression in the NAcc (Taniguchi et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

H3.3 Barcoding of Nucleus Accumbens Transcriptional Activity Identifies Novel Molecular Cascades Associated with Cocaine Self-administration in Mice

Wimmer¹,

Fant²,

Swinford-Jackson³

et al. 2019

J. Neurosci.

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Although numerous epigenetic modifications have been associated with addiction, little work has explored the turnover of histone variants. Uniquely, the H3.3 variant incorporates stably and preferentially into chromatin independently of DNA replication at active sites of transcription and transcription factor binding. Thus, genomic regions associated with H3.3-containing nucleosomes are particularly likely to be involved in plasticity, such as following repeated cocaine exposure. A recently developed mouse line expressing a neuron-specific hemagglutinin (HA)-tagged H3.3 protein was used to track transcriptionally active sites cumulatively across 19 d of cocaine self-administration. RNA-seq and H3.3-HA ChIP-seq analyses were performed on NAcc tissue collected following cocaine or food self-administration in male mice. RNA sequencing revealed five genes upregulated in cocaine relative to food self-administering mice: Fosb, Npas4, Vgf, Nptx2, and Pmepa1, which reflect known and novel cocaine plasticity-associated genes. Subsequent ChIP-seq analysis confirmed increased H3.3 aggregation at four of these five loci, thus validating H3.3 insertion as a marker of enhanced cocaine-induced transcription. Further motif recognition analysis of the ChIP-seq data showed that cocaine-associated differential H3.3 accumulation correlated with the presence of several transcription factor binding motifs, including RBPJ1, EGR1, and SOX4, suggesting that these are potentially important regulators of molecular cascades associated with cocaine-induced neuronal plasticity. Additional ontological analysis revealed differential H3.3 accumulation mainly near genes involved in neuronal differentiation and dendrite formation. These results establish the H3.3-HA transgenic mouse line as a compelling molecular barcoding tool to identify the cumulative effects of long-term environmental perturbations, such as exposure to drugs of abuse.

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Section: Discussionmentioning

confidence: 99%

H3.3 Barcoding of Nucleus Accumbens Transcriptional Activity Identifies Novel Molecular Cascades Associated with Cocaine Self-administration in Mice

Wimmer¹,

Fant²,

Swinford-Jackson³

et al. 2019

J. Neurosci.

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“…One μg of RNA was used to synthesize the cDNA by the iScript kit (Biorad, Milan, Italy) according to manufacturer's instructions. Samples were then processed for quantitative real time PCR by a CFX Connected Real-Time System (Biorad) using iTaq Universal SYBR Green Supermix (Bio-Rad) as previously described (Mallei et al, 2018). PCR cycling conditions were: 10 min at 95 °C, 40 cycles of 15 s at 95 °C and 15 s at 60 °C.…”

Section: Mrna Expression Of Kat I and Kat Iimentioning

confidence: 99%

Prenatal THC exposure raises kynurenic acid levels in the prefrontal cortex of adult rats

Beggiato

Ieraci

Tomasini

et al. 2020

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Cannabis remains one of the most widely used illicit drugs during pregnancy. The main psychoactive component of marijuana (Δ 9-tetrahydrocannabinol, THC) is correlated with untoward physiological effects in the offspring. Neurobehavioral and cognitive impairments have been reported in longitudinal studies on children and adolescents prenatally exposed to marijuana, and a link to psychiatric disorders has been proposed. Interestingly, the deleterious effects of prenatal cannabis use are similar to those observed in adult rats prenatally exposed to (L)kynurenine, the direct bioprecursor of the neuroactive metabolite kynurenic acid (KYNA). We therefore investigated whether alterations in KYNA levels in the rat brain might play a role in the long-term consequences of prenatal cannabinoid exposure. Pregnant Wistar rats were treated daily with THC [5 mg/kg, p.o.] from gestational day (GD)5 through GD20. Using in vivo microdialysis in the medial prefrontal cortex, adult animals were then used to determine the extracellular levels of KYNA and glutamate. Compared to controls, extracellular basal KYNA levels were higher, and basal glutamate levels were lower, in prenatally THC-exposed rats. These rats also showed abnormal short-term memory. Following an additional acute challenge with a low dose of *

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“…cDNA was synthesized using the iScript kit (Biorad, Milan, Italy) according to manufacturer's instructions. Quantitative Real-Time PCR analysis was performed on a CFX Connect Real Time System (Biorad) using the iTaq Universal SYBR Green supermix (Biorad), as previously described [42]. Primer sequences are described in Table 1.…”

Section: Rna Isolation and Reverse Transcription Quantitative Real-time Pcrmentioning

confidence: 99%

Apocynin Prevents Anxiety-Like Behavior and Histone Deacetylases Overexpression Induced by Sub-Chronic Stress in Mice

et al. 2021

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Anxiety disorders are common mental health diseases affecting up to 7% of people around the world. Stress is considered one of the major environmental risk factors to promote anxiety disorders through mechanisms involving epigenetic changes. Moreover, alteration in redox balance and increased reactive oxygen species (ROS) production have been detected in anxiety patients and in stressed-animal models of anxiety. Here we tested if the administration of apocynin, a natural origin antioxidant, may prevent the anxiety-like phenotype and reduction of histone acetylation induced by a subchronic forced swimming stress (FSS) paradigm. We found that apocynin prevented the enhanced latency time in the novelty-suppressed feeding test, and the production of malondialdehyde induced by FSS. Moreover, apocynin was able to block the upregulation of p47phox, a key subunit of the NADPH oxidase complex. Finally, apocynin prevented the rise of hippocampal Hdac1, Hdac4 and Hdac5, and the reduction of histone-3 acetylation levels promoted by FSS exposure. In conclusion, our results provide evidence that apocynin reduces the deleterious effect of stress and suggests that oxidative stress may regulate epigenetic mechanisms.

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Global epigenetic analysis of BDNF Val66Met mice hippocampus reveals changes in dendrite and spine remodeling genes

Cited by 14 publications

References 88 publications

H3.3 Barcoding of Nucleus Accumbens Transcriptional Activity Identifies Novel Molecular Cascades Associated with Cocaine Self-administration in Mice

H3.3 Barcoding of Nucleus Accumbens Transcriptional Activity Identifies Novel Molecular Cascades Associated with Cocaine Self-administration in Mice

Prenatal THC exposure raises kynurenic acid levels in the prefrontal cortex of adult rats

Apocynin Prevents Anxiety-Like Behavior and Histone Deacetylases Overexpression Induced by Sub-Chronic Stress in Mice

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