Gestational 1-nitropyrene exposure causes anxiety-like behavior partially by altering hippocampal epigenetic reprogramming of synaptic plasticity in male adult offspring

Wang, Bo; Zhao, Ting; Chen, Xiaoxi; Zhu, Yan-Yan; Xue, Lingxiao; Qian, Qing-Hua; Chen, Huiru; Meng, Xiu-Hong; Wang, Hua; Wei, Wei; Xu, De-Xiang

doi:10.1016/j.jhazmat.2023.131427

Cited by 7 publications

(3 citation statements)

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“…The dosage of 1‐NP referred to the previous study. [ 14 ] All pregnant mice gave birth naturally. At postnatal day (PND)28, three‐chamber test was used to evaluate autism‐like behaviors in weaning pups.…”

Section: Methodsmentioning

confidence: 99%

“…[ 12 ] Moreover, gestational 1‐NP (10, 100 µg kg −1 ) exposure during the whole pregnancy caused anxiety‐like behavior in adult stage. [ 14 ] Albeit these neurological disorders in association with 1‐NP exposure, it is still unclear whether maternal 1‐NP exposure induces autism‐like behavior in the offspring.…”

Section: Introductionmentioning

confidence: 99%

“…[ 23 , 24 ] Our previous study showed that Nrg1 could be transcriptionally regulated by modification of hydroxymethylation. [ 14 ] Thus, we hypothesized that prenatal 1‐NP exposure restrains interneuron migration through inhibiting hydroxymethylation modification of interneuron migration‐associated genes.…”

Section: Introductionmentioning

confidence: 99%

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Prenatal 1‐Nitropyrene Exposure Causes Autism‐Like Behavior Partially by Altering DNA Hydroxymethylation in Developing Brain

Zhao,

Huang,

Zhang

et al. 2024

Advanced Science

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder, characterized by social communication disability and stereotypic behavior. This study aims to investigate the impact of prenatal exposure to 1‐nitropyrene (1‐NP), a key component of motor vehicle exhaust, on autism‐like behaviors in a mouse model. Three‐chamber test finds that prenatal 1‐NP exposure causes autism‐like behaviors during the weaning period. Patch clamp shows that inhibitory synaptic transmission is reduced in medial prefrontal cortex of 1‐NP‐exposed weaning pups. Immunofluorescence finds that prenatal 1‐NP exposure reduces the number of prefrontal glutamate decarboxylase 67 (GAD67) positive interneurons in fetuses and weaning pups. Moreover, prenatal 1‐NP exposure retards tangential migration of GAD67‐positive interneurons and downregulates interneuron migration‐related genes, such as Nrg1, Erbb4, and Sema3F, in fetal forebrain. Mechanistically, prenatal 1‐NP exposure reduces hydroxymethylation of interneuron migration‐related genes through inhibiting ten‐eleven translocation (TET) activity in fetal forebrain. Supplement with alpha‐ketoglutarate (α‐KG), a cofactor of TET enzyme, reverses 1‐NP‐induced hypohydroxymethylation at specific sites of interneuron migration‐related genes. Moreover, α‐KG supplement alleviates 1‐NP‐induced migration retardation of interneurons in fetal forebrain. Finally, maternal α‐KG supplement improves 1‐NP‐induced autism‐like behaviors in weaning offspring. In conclusion, prenatal 1‐NP exposure causes autism‐like behavior partially by altering DNA hydroxymethylation of interneuron migration‐related genes in developing brain.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%