Thymol improves autism-like behaviour in VPA-induced ASD rats through the Pin1/p38 MAPK pathway

Xiong, Yang; Chen, Jianhui; Lv, Mingqi; Wang, Feifei; Zhang, Hanhong; Tang, Boyi; Li, Yingbo

doi:10.1016/j.intimp.2023.109885

Cited by 7 publications

(1 citation statement)

References 49 publications

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“…On PND 51, a three‐chamber sociability assay was performed using a transparent box (120 × 20 × 22 cm) divided by baffles into three equal chambers, as previously described. 19 , 39 , 40 , 41 The left and right chambers contained wire mesh cups, and the movements were tracked and recorded using a video recorder. Briefly, the mice were habituated for 10 min and allowed to freely explore all three chambers before the test.…”

Section: Methodsmentioning

confidence: 99%

Melatonin ameliorates sleep–wake disturbances and autism‐like behaviors in the Ctnnd2 knock out mouse model of autism spectrum disorders

Wang

et al. 2023

Genes Brain and Behavior

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Autism spectrum disorder (ASD) is a prevalent neurodevelopmental disorder characterized by atypical patterns of social interaction and communication, as well as restrictive and repetitive behaviors. In addition, patients with ASD often presents with sleep disturbances. Delta (δ) catenin protein 2 (CTNND2) encodes δ‐catenin protein, a neuron‐specific catenin implicated in many complex neuropsychiatric diseases. Our previous study demonstrated that the deletion of Ctnnd2 in mice led to autism‐like behaviors. However, to our knowledge, no study has investigated the effects of Ctnnd2 deletion on sleep in mice. In this study, we investigated whether the knockout (KO) of exon 2 of the Ctnnd2 gene could induce sleep–wake disorders in mice and identified the effects of oral melatonin (MT) supplementation on Ctnnd2 KO mice. Our results demonstrated that the Ctnnd2 KO mice exhibited ASD‐like behaviors and sleep–wake disorders that were partially attenuated by MT supplementation. Overall, our current study is the first to identify that knockdown of Ctnnd2 gene could induce sleep–wake disorders in mice and suggests that treatment of sleep–wake disturbances by MT may benefit to autism‐like behaviors causing by Ctnnd2 gene deletion.

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Section: Methodsmentioning

confidence: 99%

Melatonin ameliorates sleep–wake disturbances and autism‐like behaviors in the Ctnnd2 knock out mouse model of autism spectrum disorders

Wang

et al. 2023

Genes Brain and Behavior

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Epigenetic underpinnings of the autistic mind: Histone modifications and prefrontal excitation/inhibition imbalance

Fard,

Sadeghi,

Pajoohesh

et al. 2024

American J of Med Genetics Pt B

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Autism spectrum disorder (ASD) is complex neurobehavioral condition influenced by several cellular and molecular mechanisms that are often concerned with synaptogenesis and synaptic activity. Based on the excitation/inhibition (E/I) imbalance theory, ASD could be the result of disruption in excitatory and inhibitory synaptic transmission across the brain. The prefrontal cortex (PFC) is the chief regulator of executive function and can be affected by altered neuronal excitation and inhibition in the course of ASD. The molecular mechanisms involved in E/I imbalance are subject to epigenetic regulation. In ASD, altered enrichment and spreading of histone H3 and H4 modifications such as the activation‐linked H3K4me2/3, H3K9ac, and H3K27ac, and repression‐linked H3K9me2, H3K27me3, and H4K20me2 in the PFC result in dysregulation of molecules mediating synaptic excitation (ARC, EGR1, mGluR2, mGluR3, GluN2A, and GluN2B) and synaptic inhibition (BSN, EphA7, SLC6A1). Histone modifications are a dynamic component of the epigenetic regulatory elements with a pronounced effect on patterns of gene expression with regards to any biological process. The excitation/inhibition imbalance associated with ASD is based on the excitatory and inhibitory synaptic activity in different regions of the brain, including the PFC, the ultimate outcome of which is highly influenced by transcriptional activity of relevant genes.

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NEAT1 Promotes Valproic Acid-Induced Autism Spectrum Disorder by Recruiting YY1 to Regulate UBE3A Transcription

He,

Zhou,

Chen

et al. 2024

Mol Neurobiol

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Thymol improves autism-like behaviour in VPA-induced ASD rats through the Pin1/p38 MAPK pathway

Cited by 7 publications

References 49 publications

Melatonin ameliorates sleep–wake disturbances and autism‐like behaviors in the Ctnnd2 knock out mouse model of autism spectrum disorders

Melatonin ameliorates sleep–wake disturbances and autism‐like behaviors in the Ctnnd2 knock out mouse model of autism spectrum disorders

Epigenetic underpinnings of the autistic mind: Histone modifications and prefrontal excitation/inhibition imbalance

NEAT1 Promotes Valproic Acid-Induced Autism Spectrum Disorder by Recruiting YY1 to Regulate UBE3A Transcription

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