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Cited by 95Effects and risks of endocrine disrupting chemicalsSexual Differentiation and DisordersToxic Organic Pollutants Impact

Prenatal PCBs disrupt early neuroendocrine development of the rat hypothalamus

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Dickerson, Sarah M., Cunningham, Stephanie L., Gore, Andrea C.·2011·Toxicology and Applied Pharmacology
DOI 10.1016/j.taap.2011.01.012PMC PMC3060304
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Abstract

Neonatal exposure to endocrine disrupting chemicals (EDCs) such as polychlorinated biphenyls (PCBs) can interfere with hormone-sensitive developmental processes, including brain sexual differentiation. We hypothesized that disruption of these processes by gestational PCB exposure would be detectable as early as the day after birth (postnatal day (P) 1) through alterations in hypothalamic gene and protein expression. Pregnant Sprague-Dawley rats were injected twice, once each on gestational days 16 and 18, with one of the following: DMSO vehicle; the industrial PCB mixture Aroclor 1221 (A1221); a reconstituted mixture of the three most prevalent congeners found in humans, PCB138, PCB153, and PCB180; or estradiol benzoate (EB). On P1, litter composition, anogenital distance (AGD), and body weight were assessed. Pups were euthanized for immunohistochemistry of estrogen receptor α (ERα) or TUNEL labeling of apoptotic cells or quantitative PCR of 48 selected genes in the preoptic area (POA). We found that treatment with EB or A1221 had a sex-specific effect on developmental apoptosis in the neonatal anteroventral periventricular nucleus (AVPV), a sexually dimorphic hypothalamic region involved in the regulation of reproductive neuroendocrine function. In this region, exposed females had increased numbers of apoptotic nuclei, whereas there was no effect of treatment in males. For ERα, EB treatment increased immunoreactive cell numbers and density in the medial preoptic nucleus (MPN) of both males and females, while A1221 and the PCB mixture had no effect. PCR analysis of gene expression in the POA identified nine genes that were significantly altered by prenatal EDC exposure, in a manner that varied by sex and treatment. These genes included brain-derived neurotrophic factor, GABA(B) receptors-1 and -2, IGF-1, kisspeptin receptor, NMDA receptor subunits NR2b and NR2c, prodynorphin, and TGFα. Collectively, these results suggest that the disrupted sexual differentiation of the POA by prenatal EDC exposures is already evident as early as the day after birth, effects that may change the trajectory of postnatal development and compromise adult reproductive function.

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  • Age- and sex-specific changes in microRNA expression have been described in the developing hypothalamus of rats, suggesting PCB exposure may reprogram neuroendocrine and synaptic development through long-lasting gene-regulatory mechanisms.

    “Age- and sex-specific changes in microRNA expression have also been described in the developing hypothalamus of rats, suggesting that PCB exposure may reprogram neuroendocrine and synaptic development through long-lasting gene-regulatory mechanisms (Dickerson et al., 2011; Topper et al., 2015).”

    From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Dickerson et al., 2011

    The Results and Discussion report sex-dependent changes in neuroendocrine gene expression in the neonatal rat hypothalamus after developmental PCB exposure, with possible implications for neural circuitry. They do not report microRNA expression, age-specific microRNA changes, or a long-lasting microRNA-mediated mechanism; searches for microRNA and long-lasting gene-regulatory mechanisms found no supporting passage. (LLM, conf=0.88)

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  • Prenatal PCB exposure disrupts early hypothalamic neuroendocrine development in rats, resulting in reduced thyroid hormone levels and consequent motor deficits and sensory impairments such as hearing loss; these abnormalities can be mitigated by thyroxine replacement therapy, supporting a causal role for thyroid disruption.

    “Prenatal PCB exposure disrupts early hypothalamic neuroendocrine development in rats, resulting in reduced thyroid hormone levels and consequent motor deficits and sensory impairments such as hearing loss; notably, these abnormalities can be mitigated by thyroxine replacement therapy, supporting a causal role for thyroid disruption (Dickerson et al., 2011; Goldey and Crofton, 1998).”

    From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Dickerson et al., 2011

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  • PCBs have been associated with global DNA hypomethylation and altered microRNA expression, particularly in the developing brain.

    “PCBs have been associated with global DNA hypomethylation and altered microRNA expression, particularly in the developing brain.”

    From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Dickerson et al., 2011

    The Results and Discussion report changes in neuroendocrine gene expression in the neonatal rat hypothalamus, but do not identify those changes as microRNA expression. Searches of our full-text copy for DNA methylation and microRNA found no passage addressing either claimed association. (LLM, conf=0.77)

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Authors
Dickerson, S. M., Cunningham, S. L., & Gore, A. C.
Affiliations
The University of Texas at Austin (US)
Corresponding author
Gore, Andrea C.
ORCID
Venue
Toxicology and Applied Pharmacology
Publisher
Elsevier BV
Published
2011-04
Volume
252
Issue
1
Pages
36-46
ISSN
0041-008X (ISSN-L)
DOI
10.1016/j.taap.2011.01.012
PMC
PMC3060304
OpenAlex
W2059421349
Cited by
95
References
2
Citations by year
2026: 3 · 2025: 6 · 2024: 5 · 2023: 5 · 2022: 2 · 2021: 11 · 2020: 8 · 2019: 1 · 2018: 5 · 2017: 5 · 2016: 6 · 2015: 11 · 2014: 9 · 2013: 10 · 2012: 3
FWCI
6.25
Type
journal article
Language
en
Open access
Licence
Locations
  • Toxicology and Applied Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Science Foundation (04–615)
  • National Institutes of Health (T32 ES07247, ES07784, ES018139)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
Keywords
polychlorinated biphenyls, endocrine disruptors, prenatal exposure, hypothalamus, preoptic area, sexual differentiation of the brain, estrogen receptor alpha, apoptosis, anteroventral periventricular nucleus, anogenital distance, estradiol benzoate, Aroclor 1221, sex differences, kisspeptin receptor, NMDA receptor
MeSH terms
Age Factors, Animals, Animals, Newborn, Female, Hypothalamus, Male, Neurosecretory Systems, Polychlorinated Biphenyls, Pregnancy, Prenatal Exposure Delayed Effects, Random Allocation, Rats, Sprague-Dawley, Rats, Endocrine Disruptors

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