Maternal exposure to low dose BDE209 and Pb mixture induced neurobehavioral anomalies in C57BL/6 male offspring

Chen, Yuanhong; Liu, Shuyun; Xu, Hui; Zheng, Huiying; Bai, Chenglian; Pan, Wenhao; Zhou, Huanhuan; Liao, Min; Huang, Changjiang; Dong, Qiaoxiang

doi:10.1016/j.tox.2019.02.016

Cited by 30 publications

(21 citation statements)

References 61 publications

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“…Basic social behaviours like general sociability are among the few that show little variability across MIA studies (Kentner et al, 2019). The effect of poly I:C on general sociability and social novelty behaviours is generally robust to variation in dose, administration time, species, sex, or animal age (Chen et al, 2019;Lins et al, 2018;Lins et al, 2019;Malkova et al, 2012;Smith et al, 2007). However, the present study did not find a treatment-related effect on general sociability and social novelty preference as has been discussed in detail in section 4.6.…”

Section: Behavioural Outcomescontrasting

confidence: 41%

“…None of the juvenile groups showed a preference for the social/novel social stimulus (phase #2/3) at all. The absence of social preference in the pups' control group makes result interpretation challenging, especially as several studies have established a clear preference for the social stimulus in phase #2 (Chen et al, 2019;Lins et al, 2018;Lins et al, 2019;Malkova et al, 2012;Smith et al, 2007) and novel social stimulus in phase #3 (Chen et al, 2019). However, all aforementioned studies used adult animals and, to my knowledge, none of the published poly I:C sociability and social novelty behaviour studies used juvenile animals.…”

Section: Lack Of Preference For Social and Novel Social Stimuli In Pupsmentioning

confidence: 99%

“…The SAA paradigm is highly validated, as it has been utilised extensively in rodent research using the poly I:C model to display the deficient social interaction characteristic of autism (Crawley, 2007). Several studies used the SAA model with rodents prenatally exposed to poly I:C and found that these animals spent less time with the social stimulus than did control animals (Chen et al, 2019;Lins et al, 2018;Lins et al, 2019;Malkova et al, 2012;Smith et al, 2007). The only study that also included social novelty behaviour reported that the poly I:C group did not prefer the novel over the familiar rat (Chen et al, 2019).…”

Section: Social Noveltymentioning

confidence: 99%

“…Several studies used the SAA model with rodents prenatally exposed to poly I:C and found that these animals spent less time with the social stimulus than did control animals (Chen et al, 2019;Lins et al, 2018;Lins et al, 2019;Malkova et al, 2012;Smith et al, 2007). The only study that also included social novelty behaviour reported that the poly I:C group did not prefer the novel over the familiar rat (Chen et al, 2019). The poly I:C effect was relatively robust across differing factors such as poly I:C dose, gestational administration day, rodent type (i.e., rats or mice), sex (i.e., males and females), as well as animal age (i.e., adolescents and adults).…”

Section: Social Noveltymentioning

confidence: 99%

“…While some studies ran several habituation sessions with the stimulus mice before testing (Chen et al, 2019;Crawley, 2004;Moy et al, 2008;Nadler et al, 2004), the stimulus animals in the present study had not been habituated to the wire cups. However, other studies (Lins et al, 2018;Lins et al, 2019;Malkova et al, 2012) did not habituate the stimulus animals and yet, they found a social preference.…”

Section: Preference For the Social Stimulus In Adultsmentioning

confidence: 99%

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An Immune Rat Model of Autism: Does Environmental Enrichment Alter Higher Social Functioning?

Wilkin-Krug¹

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The neurodevelopmental condition autism spectrum disorder (ASD) is marked by impaired communication, impaired social interaction, and repetitive or restricted behaviours (American Psychiatric Association, 2013). ASD is caused by a combination of genetic and environmental factors, including maternal infection during pregnancy. There are no pharmacological treatment options for ASD, but environmental enrichment (EE) is a promising alternative to rehabilitate or prevent related symptoms. Patients with ASD often have a deficit in higher social abilities, including prosociality, but to date, no rat studies have investigated how EE affects higher social functions in the context of ASD. Therefore, this thesis investigated the effect of EE on higher social functions in an in vivo rodent model of ASD. Using a two-by-two factorial design, pregnant Sprague Dawley rats received either saline or the viral mimic polyinosinic-polycytidylic acid (poly I:C) to trigger an immune reaction and were placed in either standard or enriched housing. In the enrichment groups, pups received pre-weaning enrichment sessions while animals in the standard-housing groups were left undisturbed until weaning. I assessed the animals’ neonatal communication, general sociability and social novelty behaviour, prosocial tendencies, and locomotor activity. The main hypothesis I investigated was that the maternal immune reaction would disrupt fetal neural development and alter communication and social behaviours in the offspring and that EE would reduce or reverse these deficits. There was a transient poly I:C effect on neonatal communication early on, but the treatment did not cause long-term social deficits. Poly I:C also affected adult locomotor activity but did neither reduce sociability nor prosociality. As the very weak treatment effects did not result in clear deficits, EE could not lead to improvements. While the findings did not offer insight into the enrichment effect on impaired prosocial behaviours, this was likely due to methodological issues and limitations. Future ASD research should address these concerns to further the understanding of how environmental adjustments can stimulate the impaired social parts of the brain to redirect the atypical developmental trajectory towards a more typical one.

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Section: Behavioural Outcomescontrasting

confidence: 41%

Section: Lack Of Preference For Social and Novel Social Stimuli In Pupsmentioning

confidence: 99%

Section: Social Noveltymentioning

confidence: 99%

Section: Social Noveltymentioning

confidence: 99%

Section: Preference For the Social Stimulus In Adultsmentioning

confidence: 99%

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An Immune Rat Model of Autism: Does Environmental Enrichment Alter Higher Social Functioning?

Wilkin-Krug¹

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Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

Mao,

Tang,

et al. 2024

Environmental Toxicology

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Decabrominated diphenyl ether (BDE‐209) is a typical persistent organic pollutant that can cross the placental barrier, increasing the exposure risk for offspring. Norepinephrine (NE) from nerve terminals and acetylcholine (Ach) can bind to specific receptors on immune cells, inhibit the immune function of the body then cause immunotoxicity. However, whether maternal exposure to BDE‐209 could lead to immunotoxicity in the offspring by acting on the sympathetic and parasympathetic nervous systems remains unclear. In view of this, the pregnancy and lactation rat BDE‐209 exposure model was established and the results demonstrated that pregnancy and lactation BDE‐209 exposure could induce immunotoxicity to female offspring via affecting immunopathology (hematological and biochemical parameters, organ indices, and spleen histopathological), decreasing humoral immunity (serum hemolysin, immunoglobulins, and cytokine productions), damaging cellular immunity (splenic lymphocytes and spleen cytokine productions), and restraining nonspecific immunity. Moreover, a dramatically significant correlation was observed between spleen nerve indices and immunity indices. Additionally, the mechanism revealed that maternal BDE‐209 exposure caused offspring immunotoxicity through (1) activating MHC/PKCθ/NF‐κB pathway; (2) promoting sympathetic nervous pathway, by upregulating the expression of β2AR protein, which in turn elevating cAMP, following activate PKA and phosphorylate CREB, ultimately leading to immunotoxicity;(3) activating parasympathetic nerve pathway by reducing the binding with Ach and α7nAchR, upregulating the expression of JAK2 and phosphorylating STAT3, induced immunotoxicity of female offspring.

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Persistent autism-relevant behavioral phenotype and social neuropeptide alterations in female mice offspring induced by maternal transfer of PBDE congeners in the commercial mixture DE-71

et al. 2021

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Polybrominated diphenyl ethers (PBDEs) are ubiquitous persistent organic pollutants (POPs) that are known neuroendocrine disrupting chemicals with adverse neurodevelopmental effects. PBDEs may act as risk factors for autism spectrum disorders (ASD), characterized by abnormal psychosocial functioning, although direct evidence is currently lacking. Using a translational exposure model, we tested the hypothesis that maternal transfer of a commercial mixture of PBDEs, DE-71, produces ASD-relevant behavioral and neurochemical deficits in female offspring. C57Bl6/N mouse dams (F0) were exposed to DE-71 via oral administration of 0 (VEH/CON), 0.1 (L-DE-71) or 0.4 (H-DE-71) mg/kg bw/d from 3 wk prior to gestation through end of lactation. Mass spectrometry analysis indicated in utero and lactational transfer of PBDEs (in ppb) to F1 female offspring brain tissue at postnatal day (PND) 15 which was reduced by PND 110. Neurobehavioral testing of social novelty preference (SNP) and social recognition memory (SRM) revealed that adult L-DE-71 F1 offspring display deficient short- and long-term SRM, in the absence of reduced sociability, and increased repetitive behavior. These effects were concomitant with reduced olfactory discrimination of social odors. Additionally, L-DE-71 exposure also altered short-term novel object recognition memory but not anxiety or depressive-like behavior. Moreover, F1 L-DE-71 displayed downregulated mRNA transcripts for oxytocin (Oxt) in the bed nucleus of the stria terminalis (BNST) and supraoptic nucleus, and vasopressin (Avp) in the BNST and upregulated Avp1ar in BNST, and Oxtr in the paraventricular nucleus. Our work demonstrates that developmental PBDE exposure produces ASD-relevant neurochemical, olfactory processing and behavioral phenotypes that may result from early neurodevelopmental reprogramming within central social and memory networks.

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Maternal exposure to low dose BDE209 and Pb mixture induced neurobehavioral anomalies in C57BL/6 male offspring

Cited by 30 publications

References 61 publications

An Immune Rat Model of Autism: Does Environmental Enrichment Alter Higher Social Functioning?

An Immune Rat Model of Autism: Does Environmental Enrichment Alter Higher Social Functioning?

Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

Persistent autism-relevant behavioral phenotype and social neuropeptide alterations in female mice offspring induced by maternal transfer of PBDE congeners in the commercial mixture DE-71

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