Hyperactivity of basolateral amygdala mediates behavioral deficits in mice following exposure to bisphenol A and its analogue alternative

Hu, Fan; Liang, Weifeng; Zhang, Linke; Wang, Huan; Li, Zimu; Zhou, Yifeng

doi:10.1016/j.chemosphere.2021.132044

Cited by 10 publications

(7 citation statements)

References 59 publications

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“…Chen et al also found that the behavioral changes in methamphetamine-exposed mice are associated with the reduction in SCFAs that is linked to inflammation and epigenetic modification [117]. Bisphenol A (BPA) is considered to be another environmental factor (in fact a contaminant) that may affect the neurobehavioral system during childhood and adulthood periods owing to its extensive use in the production of polycarbonate plastics and epoxy resins such as food or water containers, dental sealants, and thermal papers [118][119][120][121]. Although BPA is known to reduce global DNA methylation [122], altering neurogenesis following in vivo maternal and in vitro BPA exposure has been attributed to an increase in the epigenetic regulator lysine-specific histone For example, acetate production from the breakdown of alcohol gives rise to dynamic acetylation of histones in the brain tissue.…”

Section: Maternal Diet Offspring Gut Microbiome and Brain Functionsmentioning

confidence: 99%

Epigenetic Aberrations in Major Psychiatric Diseases Related to Diet and Gut Microbiome Alterations

Nohesara

Abdolmaleky

Thiagalingam

2023

Genes

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Nutrition and metabolism modify epigenetic signatures like histone acetylation and DNA methylation. Histone acetylation and DNA methylation in the central nervous system (CNS) can be altered by bioactive nutrients and gut microbiome via the gut–brain axis, which in turn modulate neuronal activity and behavior. Notably, the gut microbiome, with more than 1000 bacterial species, collectively contains almost three million functional genes whose products interact with millions of human epigenetic marks and 30,000 genes in a dynamic manner. However, genetic makeup shapes gut microbiome composition, food/nutrient metabolism, and epigenetic landscape, as well. Here, we first discuss the effect of changes in the microbial structure and composition in shaping specific epigenetic alterations in the brain and their role in the onset and progression of major mental disorders. Afterward, potential interactions among maternal diet/environmental factors, nutrition, and gastrointestinal microbiome, and their roles in accelerating or delaying the onset of severe mental illnesses via epigenetic changes will be discussed. We also provide an overview of the association between the gut microbiome, oxidative stress, and inflammation through epigenetic mechanisms. Finally, we present some underlying mechanisms involved in mediating the influence of the gut microbiome and probiotics on mental health via epigenetic modifications.

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Section: Maternal Diet Offspring Gut Microbiome and Brain Functionsmentioning

confidence: 99%

Epigenetic Aberrations in Major Psychiatric Diseases Related to Diet and Gut Microbiome Alterations

Nohesara

Abdolmaleky

Thiagalingam

2023

Genes

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“…BLA sends several outputs to the central nucleus (CeA) and the medial nucleus (MeA), which in turn project to other brain areas that will be responsible for triggering adaptative behaviors to facing stress [ 5 ]. As mentioned before, the amygdala receives inhibitory projections from the IL mPFC, which can be weakened after stressful situations, resulting in a lack of inhibition of BLA by the PFC and hyperactivation of the amygdala [ 24 , 25 ]. For instance, depressed and PTSD patients have bigger and more active amygdala than healthy volunteers [ 26–28 ].…”

Section: Overview Of Stress Response and Circuitrymentioning

confidence: 99%

Endocannabinoid signaling and epigenetics modifications in the neurobiology of stress-related disorders

et al. 2023

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Stress exposure is associated with psychiatric conditions, such as depression, anxiety, and post-traumatic stress disorder (PTSD). It is also a vulnerability factor to developing or reinstating substance use disorder. Stress causes several changes in the neuro-immune-endocrine axis, potentially resulting in prolonged dysfunction and diseases. Changes in several transmitters, including serotonin, dopamine, glutamate, GABA, glucocorticoids, and cytokines, are associated with psychiatric disorders or behavioral alterations in preclinical studies. Complex and interacting mechanisms make it very difficult to understand the physiopathology of psychiatry conditions; therefore, studying regulatory mechanisms that impact these alterations is a good approach. In the last decades, the impact of stress on biology through epigenetic markers, which directly impact gene expression, is under intense investigation; these mechanisms are associated with behavioral alterations in animal models after stress or drug exposure, for example. The endocannabinoid (eCB) system modulates stress response, reward circuits, and other physiological functions, including HPA axis activation and immune response. eCBs, for example, act retrogradely at presynaptic neurons, limiting the release of neurotransmitters, a mechanism implicated in the antidepressant and anxiolytic effects after stress. Epigenetic mechanisms can impact the expression of eCB system molecules, which in turn can regulate epigenetic mechanisms. This review will present evidence of how the eCB system and epigenetic mechanisms interact and the consequences of this interaction in modulating behavioral changes after stress exposure in preclinical studies or psychiatric conditions. Moreover, evidence that correlates the involvement of the eCB system and epigenetic mechanisms in drug abuse contexts will be discussed.

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“…Amygdala is an almond‐shaped cluster of nuclei located deeply and medially within the temporal lobes of the brain in complex vertebrates and modulates emotion, mood, memory, and cognition. The basolateral amygdala (BLA), which is divided into the lateral amygdala (LA) and basal amygdala (BA), as one of the main component of the amygdala, plays an important role in the regulation of emotion, memory, and anxiety disorders 1–3 . Altered the excitability of glutamatergic neurons in BLA is surveyed in the pathophysiology of anxiety, depression, memory impairments, and post‐traumatic stress disorders (PTSDs) 4,5 .…”

Section: Introductionmentioning

confidence: 99%

“…The basolateral amygdala (BLA), which is divided into the lateral amygdala (LA) and basal amygdala (BA), as one of the main component of the amygdala, plays an important role in the regulation of emotion, memory, and anxiety disorders. 1 , 2 , 3 Altered the excitability of glutamatergic neurons in BLA is surveyed in the pathophysiology of anxiety, depression, memory impairments, and post‐traumatic stress disorders (PTSDs). 4 , 5 Fear memory has attracted much attention because of its close relationship with psychological trauma.…”

Section: Introductionmentioning

confidence: 99%

MPP2 interacts with SK2 to rescue the excitability of glutamatergic neurons in the BLA and facilitate the extinction of conditioned fear in mice

et al. 2023

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AimsThe basolateral amygdala (BLA) plays an integral role in anxiety disorders (such as post traumatic stress disorder) stem from dysregulated fear memory. The excitability of glutamatergic neurons in the BLA correlates with fear memory, and the afterhyperpolarization current (IAHP) mediated by small‐conductance calcium‐activated potassium channel subtype 2 (SK2) dominates the excitability of glutamatergicneurons. This study aimed to explore the effect of MPP2 interacts with SK2 in the excitability of glutamatergic neurons in the BLA and the extinction of conditioned fear in mice.MethodsFear memory was analyzed via freezing percentage. Western blotting and fluorescence quantitative PCR were used to determine the expression of protein and mRNA respectively. Electrophysiology was employed to measure the excitability of glutamatergic neurons and IAHP.ResultsFear conditioning decreased the levels of synaptic SK2 channels in the BLA, which were restored following fear extinction. Notably, reduced expression of synaptic SK2 channels in the BLA during fear conditioning was caused by the increased activity of protein kinase A (PKA), while increased levels of synaptic SK2 channels in the BLA during fear extinction were mediated by interactions with membrane‐palmitoylated protein 2 (MPP2).ConclusionsOur results revealed that MPP2 interacts with the SK2 channels and rescues the excitability of glutamatergic neurons by increasing the expression of synaptic SK2 channels in the BLA to promote the normalization of anxiety disorders and provide a new direction for the treatment.

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Hyperactivity of basolateral amygdala mediates behavioral deficits in mice following exposure to bisphenol A and its analogue alternative

Cited by 10 publications

References 59 publications

Epigenetic Aberrations in Major Psychiatric Diseases Related to Diet and Gut Microbiome Alterations

Epigenetic Aberrations in Major Psychiatric Diseases Related to Diet and Gut Microbiome Alterations

Endocannabinoid signaling and epigenetics modifications in the neurobiology of stress-related disorders

MPP2 interacts with SK2 to rescue the excitability of glutamatergic neurons in the BLA and facilitate the extinction of conditioned fear in mice

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