Prenatal Stress Leads to the Altered Maturation of Corticostriatal Synaptic Plasticity and Related Behavioral Impairments Through Epigenetic Modifications of Dopamine D2 Receptor in Mice

Li, Yingchun; Jiang, Rong; Zhong, Haiquan; Min, Liang; Zhu, Chunting; Fei, Chang; Zhou, Rong

doi:10.1007/s12035-020-02127-6

Cited by 9 publications

(3 citation statements)

References 43 publications

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“…One possible mechanism for this relationship is that epigenetic aging may affect the expression of genes that are involved in neuronal function, survival, and repair. For example, epigenetic aging may alter the expression of genes that regulate inflammation (23), oxidative stress (24), synaptic plasticity (25), and neurogenesis (26). Additionally, neurodegenerative diseases may also cause acceleration of epigenetic aging.…”

Section: Discussionmentioning

confidence: 99%

The effect of epigenetic aging on neurodegenerative diseases: a Mendelian randomization study

Fan,

Liu,

Liu

et al. 2024

Front. Endocrinol.

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BackgroundAging has always been considered as a risk factor for neurodegenerative diseases, but there are individual differences and its mechanism is not yet clear. Epigenetics may unveil the relationship between aging and neurodegenerative diseases.MethodsOur study employed a bidirectional two-sample Mendelian randomization (MR) design to assess the potential causal association between epigenetic aging and neurodegenerative diseases. We utilized publicly available summary datasets from several genome-wide association studies (GWAS). Our investigation focused on multiple measures of epigenetic age as potential exposures and outcomes, while the occurrence of neurodegenerative diseases served as potential exposures and outcomes. Sensitivity analyses confirmed the accuracy of the results.ResultsThe results show a significant decrease in risk of Parkinson’s disease with GrimAge (OR = 0.8862, 95% CI 0.7914–0.9924, p = 0.03638). Additionally, we identified that HannumAge was linked to an increased risk of Multiple Sclerosis (OR = 1.0707, 95% CI 1.0056–1.1401, p = 0.03295). Furthermore, we also found that estimated plasminogen activator inhibitor-1(PAI-1) levels demonstrated an increased risk for Alzheimer’s disease (OR = 1.0001, 95% CI 1.0000–1.0002, p = 0.04425). Beyond that, we did not observe any causal associations between epigenetic age and neurodegenerative diseases risk.ConclusionThe findings firstly provide evidence for causal association of epigenetic aging and neurodegenerative diseases. Exploring neurodegenerative diseases from an epigenetic perspective may contribute to diagnosis, prognosis, and treatment of neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

The effect of epigenetic aging on neurodegenerative diseases: a Mendelian randomization study

Fan,

Liu,

Liu

et al. 2024

Front. Endocrinol.

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“…Hippocampal synaptic plasticity is closely related to cognitive function and is heavily reliant on the BDNF/TrkB signaling pathway, which regulates dendritic growth, neurogenesis, synaptic maturation, synaptic transmission, and synaptic protein synthesis (Liu et al, 2023;Wang et al, 2023). It is well known that prenatal stress interferes with synaptic pruning and synaptic plasticity in the hippocampus through environmental factors and brain counteractions via epigenetic mechanisms (Dong et al, 2018;Li et al, 2021). The BDNF/TrkB signaling pathway has been downregulated in rats exposed to maternal restraint stress accompanied by spatial learning and memory and working memory deficits (Zheng et al, 2020).…”

Section: Melatonin Improved Msd-induced Synaptic Dysfunction In the H...mentioning

confidence: 99%

Melatonin improves maternal sleep deprivation‐induced learning and memory impairment, inflammation, and synaptic dysfunction in murine male adult offspring

Zhang,

Wei,

et al. 2024

Brain and Behavior

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IntroductionMaternal sleep deprivation (MSD), which induces inflammation and synaptic dysfunction in the hippocampus, has been associated with learning and memory impairment in offspring. Melatonin (Mel) has been shown to have anti‐inflammatory, antioxidant, and neuroprotective function. However, the beneficial effect of Mel on MSD‐induced cognitive impairment and its mechanisms are unknown.MethodsIn the present study, adult offspring suffered from MSD were injected with Mel (20 mg/kg) once a day during postnatal days 61–88. The cognitive function was evaluated by the Morris water maze test. Levels of proinflammatory cytokines were examined by enzyme‐linked immunosorbent assay. The mRNA and protein levels of synaptic plasticity associated proteins were examined using reverse transcription‐polymerase chain reaction and western blotting.ResultsThe results showed that MSD impaired learning and memory in the offspring mice. MSD increased the levels of interleukin (IL)‐1creIL‐6, and tumor necrosis factor‐α and decreased the expression levels of brain‐derived neurotrophic factor, tyrosine kinase receptor B, postsynaptic density protein‐95, and synaptophysin in the hippocampus. Furthermore, Mel attenuated cognitive impairment and restored markers of inflammation and synaptic plasticity to control levels.ConclusionsThese findings indicated that Mel could ameliorate learning and memory impairment induced by MSD, and these beneficial effects were related to improvement in inflammation and synaptic dysfunction.

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“…The gastrointestinal tract, which is the largest immunological and metabolic organ in humans, comprises a range of intestinal flora that are thought to be crucial participants in the coordination of host physiology and disease ( Qin et al, 2010 ). A number of factors, including nutrition, seasonality, lifestyle, stress, usage of antibiotics, or illness, can have an impact on intestinal flora ( Li et al, 2021 ). Intestinal flora is a crucial element of human microecology and plays a crucial role in human immunity, metabolic equilibrium, and the prevention of pathogenic invasion, according to recent studies ( Glenwright et al, 2017 ; Khosravi et al, 2014 ; Pickard et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

The effects of chronic unpredicted mild stress on maternal negative emotions and gut microbiota and metabolites in pregnant rats

Wang

Zhao

et al. 2023

PeerJ

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Background Chronic long-term stress is associated with a range of disorders, including depression and a variety of other chronic illnesses. It is well known that maternal exposure to psychosocial stress during pregnancy significantly increases the likelihood of adverse pregnancy outcomes. The gut microbiota has been a popular topic, it is a key mediator of the gut-brain axis and plays an important role in human health; changes in the gut microbiota have been related to chronic stress-induced health impairment, however, the relationship between maternal negative emotions and abnormal gut microbiota and its metabolites during maternal exposure to chronic stress during pregnancy remains unclear. Methods Pregnant rats were subjected to chronic unpredicted mild stress (CUMS) to establish the rat model of chronic stress during pregnancy. The behavioral changes were recorded using sucrose preference test (SPT) and open-field test (OFT), plasma corticosterone levels were determined by radioimmunoassay, and a comprehensive method combining 16S rRNA gene sequencing and gas chromatography-mass spectrometry (GC-MS) metabolomics was used to study the effects of stress during pregnancy on the function of intestinal microbiota and its metabolites. Results Chronic stress during pregnancy not only increased maternal plasma corticosterone (P < 0.05), but also caused maternal depression-like behaviors (P < 0.05). Chronic stress during pregnancy changed the species composition at the family level of maternal gut microbiota, the species abundance of Ruminococcaceae in the stress group (23.45%) was lower than the control group (32.67%) and the species abundance of Prevotellaceae in the stress group (10.45%) was higher than the control group (0.03%) (P < 0.05). Vertical locomotion and 1% sucrose preference percentage in pregnant rats were negatively correlated with Prevotellaceae (r = − 0.90, P < 0.05). Principal component analysis with partial least squares discriminant analysis showed that the integration points of metabolic components in the stress and control groups were completely separated, indicating that there were significant differences in the metabolic patterns of the two groups, and there were seven endogenous metabolites that differed (P < 0.05). Conclusions The negative emotional behaviors that occur in pregnant rats as a result of prenatal chronic stress may be associated with alterations in the gut microbiota and its metabolites. These findings provide a basis for future targeted metabolomics and gut flora studies on the effects of chronic stress during pregnancy on gut flora.

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Prenatal Stress Leads to the Altered Maturation of Corticostriatal Synaptic Plasticity and Related Behavioral Impairments Through Epigenetic Modifications of Dopamine D2 Receptor in Mice

Cited by 9 publications

References 43 publications

The effect of epigenetic aging on neurodegenerative diseases: a Mendelian randomization study

The effect of epigenetic aging on neurodegenerative diseases: a Mendelian randomization study

Melatonin improves maternal sleep deprivation‐induced learning and memory impairment, inflammation, and synaptic dysfunction in murine male adult offspring

The effects of chronic unpredicted mild stress on maternal negative emotions and gut microbiota and metabolites in pregnant rats

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