A platform for research: civil engineering, architecture and urbanism
A platform for research: civil engineering, architecture and urbanism
Maternal Exposure of SD Rats to Benzo[a]Pyrene Impairs Neurobehavior and Hippocampal Synaptic Ultrastructure in Offspring via Downregulating Synaptic‐Associated Factors
https://orcid.org/0000-0003-4351-2017
ABSTRACTBenzo[a]pyrene (B[a]P) is a carcinogenic contaminant widely present in the environment. Recently, increasing studies have paid attention to the developmental neurotoxicity of B[a]P in offspring in their early life stages; however, the underlying molecular mechanisms have not been clearly elucidated. In this study, we aimed to evaluate the effects of prenatal B[a]P exposure on neurobehavior of pups during their brain growth spurt (BGS) period and also explore the potential underlying mechanisms. Pregnant Sprague‐Dawley (SD) rats were intraperitoneally exposed to 0, 10, 20, or 40 mg/kg‐bw B[a]P for three consecutive days during embryonic days 17–19. The physiological development index of pups was observed, and a series of neurobehavioral tests assessing sensory and motor maturation were performed. The complexity of dendritic branches and the basal dendritic spine density of CA1 pyramidal neurons were examined using Golgi‐Cox staining during PND 1–14. In addition, the mRNA and protein expression levels of hippocampal BDNF, SYP, Arc, PSD‐95, DNMT1, and DNMT3a, and the level of 5‐mC were detected using RT‐qPCR, Western blotting, or immunohistochemical staining, respectively. We noted that prenatal B[a]P exposure induced body weight loss and neurobehavioral impairments in the early life stages. Furthermore, this study firstly revealed that maternal exposure to B[a]P impaired the dendritic arborization and complexity of pyramidal neurons in the hippocampus CA1 subfield in offspring during the early postnatal period, and the damage of B[a]P to basal dendritic spine density was also observed in a dose‐dependent manner. Correspondingly, maternal exposure to B[a]P markedly reduced BDNF, Arc, SYP, and PSD‐95 mRNA and protein levels in the offspring hippocampus. Meanwhile, the levels of hippocampal DNMT1, DNMT3a, and 5‐mC significantly increased in the offspring prenatally exposed to B[a]P. In summary, this study firstly demonstrated that maternal B[a]P exposure induced neurobehavioral deficits by destroying the hippocampal synaptic ultrastructure, which was possibly associated with the downregulation of BDNF, Arc, SYP, and PSD95 in the hippocampus through increased DNMTs‐mediated DNA methylation in offspring during the BGS period.
Maternal Exposure of SD Rats to Benzo[a]Pyrene Impairs Neurobehavior and Hippocampal Synaptic Ultrastructure in Offspring via Downregulating Synaptic‐Associated Factors
https://orcid.org/0000-0003-4351-2017
ABSTRACTBenzo[a]pyrene (B[a]P) is a carcinogenic contaminant widely present in the environment. Recently, increasing studies have paid attention to the developmental neurotoxicity of B[a]P in offspring in their early life stages; however, the underlying molecular mechanisms have not been clearly elucidated. In this study, we aimed to evaluate the effects of prenatal B[a]P exposure on neurobehavior of pups during their brain growth spurt (BGS) period and also explore the potential underlying mechanisms. Pregnant Sprague‐Dawley (SD) rats were intraperitoneally exposed to 0, 10, 20, or 40 mg/kg‐bw B[a]P for three consecutive days during embryonic days 17–19. The physiological development index of pups was observed, and a series of neurobehavioral tests assessing sensory and motor maturation were performed. The complexity of dendritic branches and the basal dendritic spine density of CA1 pyramidal neurons were examined using Golgi‐Cox staining during PND 1–14. In addition, the mRNA and protein expression levels of hippocampal BDNF, SYP, Arc, PSD‐95, DNMT1, and DNMT3a, and the level of 5‐mC were detected using RT‐qPCR, Western blotting, or immunohistochemical staining, respectively. We noted that prenatal B[a]P exposure induced body weight loss and neurobehavioral impairments in the early life stages. Furthermore, this study firstly revealed that maternal exposure to B[a]P impaired the dendritic arborization and complexity of pyramidal neurons in the hippocampus CA1 subfield in offspring during the early postnatal period, and the damage of B[a]P to basal dendritic spine density was also observed in a dose‐dependent manner. Correspondingly, maternal exposure to B[a]P markedly reduced BDNF, Arc, SYP, and PSD‐95 mRNA and protein levels in the offspring hippocampus. Meanwhile, the levels of hippocampal DNMT1, DNMT3a, and 5‐mC significantly increased in the offspring prenatally exposed to B[a]P. In summary, this study firstly demonstrated that maternal B[a]P exposure induced neurobehavioral deficits by destroying the hippocampal synaptic ultrastructure, which was possibly associated with the downregulation of BDNF, Arc, SYP, and PSD95 in the hippocampus through increased DNMTs‐mediated DNA methylation in offspring during the BGS period.
Maternal Exposure of SD Rats to Benzo[a]Pyrene Impairs Neurobehavior and Hippocampal Synaptic Ultrastructure in Offspring via Downregulating Synaptic‐Associated Factors
https://orcid.org/0000-0003-4351-2017
ABSTRACTBenzo[a]pyrene (B[a]P) is a carcinogenic contaminant widely present in the environment. Recently, increasing studies have paid attention to the developmental neurotoxicity of B[a]P in offspring in their early life stages; however, the underlying molecular mechanisms have not been clearly elucidated. In this study, we aimed to evaluate the effects of prenatal B[a]P exposure on neurobehavior of pups during their brain growth spurt (BGS) period and also explore the potential underlying mechanisms. Pregnant Sprague‐Dawley (SD) rats were intraperitoneally exposed to 0, 10, 20, or 40 mg/kg‐bw B[a]P for three consecutive days during embryonic days 17–19. The physiological development index of pups was observed, and a series of neurobehavioral tests assessing sensory and motor maturation were performed. The complexity of dendritic branches and the basal dendritic spine density of CA1 pyramidal neurons were examined using Golgi‐Cox staining during PND 1–14. In addition, the mRNA and protein expression levels of hippocampal BDNF, SYP, Arc, PSD‐95, DNMT1, and DNMT3a, and the level of 5‐mC were detected using RT‐qPCR, Western blotting, or immunohistochemical staining, respectively. We noted that prenatal B[a]P exposure induced body weight loss and neurobehavioral impairments in the early life stages. Furthermore, this study firstly revealed that maternal exposure to B[a]P impaired the dendritic arborization and complexity of pyramidal neurons in the hippocampus CA1 subfield in offspring during the early postnatal period, and the damage of B[a]P to basal dendritic spine density was also observed in a dose‐dependent manner. Correspondingly, maternal exposure to B[a]P markedly reduced BDNF, Arc, SYP, and PSD‐95 mRNA and protein levels in the offspring hippocampus. Meanwhile, the levels of hippocampal DNMT1, DNMT3a, and 5‐mC significantly increased in the offspring prenatally exposed to B[a]P. In summary, this study firstly demonstrated that maternal B[a]P exposure induced neurobehavioral deficits by destroying the hippocampal synaptic ultrastructure, which was possibly associated with the downregulation of BDNF, Arc, SYP, and PSD95 in the hippocampus through increased DNMTs‐mediated DNA methylation in offspring during the BGS period.
Maternal Exposure of SD Rats to Benzo[a]Pyrene Impairs Neurobehavior and Hippocampal Synaptic Ultrastructure in Offspring via Downregulating Synaptic‐Associated Factors
Environmental Toxicology
Zhang, Yu (author) / Guo, Yuting (author) / Du, Linhu (author) / Zhao, Junxiu (author) / Ci, Xiaorui (author) / Yin, Jinzhu (author) / Niu, Qiao (author) / Mo, Yiqun (author) / Zhang, Qunwei (author) / Nie, Jisheng (author)
2025-02-18
Article (Journal)
Electronic Resource
English
| Wiley | 2021