Bisphenol-A Exposure during Gestation and Lactation Causes Visual Perception Deficits in Rat Pups Following a Decrease in Interleukin 1β Expression in the Primary Visual Cortex

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

doi:10.1016/j.neuroscience.2020.03.035

Cited by 6 publications

(11 citation statements)

References 44 publications

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Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

“…BPA-associated changes in synaptic plasticity have also been identified in the primary visual cortex [101], basal ganglia [103], and basolateral amygdala (BLA) [102] of rats. In the primary visual cortex, reductions in spine density were observed in response to low BPA exposure levels (1 mg/kg/day) [101]. In this case, the reduced spine density was connected to diminished expression of the proinflammatory cytokine, interleukin 1β (IL-1β) [101], which plays a role in LTP [111].…”

Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

“…The density of dendritic spines changes in response to neural activity; long-term potentiation (LTP) increases spine density [97], whereas long-term depression (LTD) reduces spine density [98]. Chemical exposures can disrupt synaptic plasticity by altering the expression or activity of proteins important for either structural changes in dendritic spines or neuronal signaling pathways that contribute to LTP and LTD. Maternal exposure to BPA has been found to affect the synaptic plasticity of offspring in various brain regions by reducing dendritic spine density [99][100][101], altering LTP and LTD [102,103], and dysregulating the expression of molecular regulators of plasticity (Table 3) [100][101][102][103][104][105][106].…”

Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

“…In the primary visual cortex, reductions in spine density were observed in response to low BPA exposure levels (1 mg/kg/day) [101]. In this case, the reduced spine density was connected to diminished expression of the proinflammatory cytokine, interleukin 1β (IL-1β) [101], which plays a role in LTP [111]. In the basal ganglia, low dose BPA (20 μg/kg/day) caused deficits in the development of LTP and LTD at the dorsolateral striatum via enhancement of dopamine receptor (D1R) activity, a disruption suggested by the authors to diminish control of motor behaviors [103], though it is worth noting the basal ganglia is also critical for non-motor functions, like emotion and executive function [112].…”

Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

“…Imbalances in neural excitation and inhibition have been reported in the pathophysiology of many Several recent reviews have also discussed neurobehavioral ramifications of BPA exposure in animal models [146][147][148][149][150]. Although not reviewed here, many other behaviors have been associated with early BPA exposure, including visual perception [101,128], depression-like behavior [141,151], and social and reproductive behaviors [142,147,152].…”

Section: Behavior Is Impacted By Bpamentioning

confidence: 99%

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Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

Welch¹,

Mulligan²

2022

Preprint

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Substantial evidence indicates that bisphenol A (BPA), a ubiquitous environmental chemical used in the synthesis of polycarbonate plastics and epoxy resins, can impair brain development. Clinical and epidemiological studies exploring potential connections between BPA and neurodevelopmental disorders in humans have repeatedly identified correlations between early BPA exposure and developmental disorders, like attention deficit/hyperactivity disorder and autism spectrum disorder. Investigations using invertebrate and vertebrate animal models have revealed that developmental exposure to BPA can impair multiple aspects of neuronal development, including neural stem cell proliferation and differentiation, synapse formation, and synaptic plasticity—neuronal phenotypes that are thought to underpin the fundamental changes in behavior associated neurodevelopmental disorders. Consistent with BPA-associated neuronal phenotypes, behavioral analyses of BPA-treated animals have shown significant impacts on behavioral endophenotypes related to neurodevelopmental disorders, including altered locomotor activity, learning and memory deficits, and anxiety-like behavior. To contextualize the correlations between BPA and neurodevelopmental disorders in humans, this review summarizes current literature reporting on the developmental neurotoxicity of BPA in laboratory animals, with an emphasis on neuronal phenotypes, molecular mechanisms, and behavioral outcomes. The collective works described here predominantly support the notion that gestational exposure to BPA should be regarded as a risk factor for neurodevelopmental disorders.

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Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

Section: Synaptic Plasticity Is Impaired By Bpamentioning

confidence: 99%

Section: Behavior Is Impacted By Bpamentioning

confidence: 99%

See 3 more Smart Citations

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

Welch¹,

Mulligan²

2022

Preprint

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Developmental Exposure to Bisphenol a Degrades Auditory Cortical Processing in Rats

Tang

Cheng

et al. 2022

Neurosci. Bull.

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Developmental Programming in Animal Models: Critical Evidence of Current Environmental Negative Changes

et al. 2022

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The Developmental Origins of Health and Disease (DOHaD) approach answers questions surrounding the early events suffered by the mother during reproductive stages that can either partially or permanently influence the developmental programming of children, predisposing them to be either healthy or exhibit negative health outcomes in adulthood. Globally, vulnerable populations tend to present high obesity rates, including among school-age children and women of reproductive age. In addition, adults suffer from high rates of diabetes, hypertension, cardiovascular, and other metabolic diseases. The increase in metabolic outcomes has been associated with the combination of maternal womb conditions and adult lifestylerelated factors such as malnutrition and obesity, smoking habits, and alcoholism. However, to date, "new environmental changes" have recently been considered negative factors of development, such as maternal sedentary lifestyle, lack of maternal attachment during lactation, overcrowding, smog, overurbanization, industrialization, noise pollution, and psychosocial stress experienced during the current SARS-CoV-2 pandemic. Therefore, it is important to recognize how all these factors impact offspring development during pregnancy and lactation, a period in which the subject cannot protect itself from these mechanisms. This review aims to introduce the importance of studying DOHaD, discuss classical programming studies, and address the importance of studying new emerging programming mechanisms, known as actual lifestyle factors, during pregnancy and lactation.

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Bisphenol-A Exposure during Gestation and Lactation Causes Visual Perception Deficits in Rat Pups Following a Decrease in Interleukin 1β Expression in the Primary Visual Cortex

Cited by 6 publications

References 44 publications

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

Developmental Exposure to Bisphenol a Degrades Auditory Cortical Processing in Rats

Developmental Programming in Animal Models: Critical Evidence of Current Environmental Negative Changes

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