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

Autor: Jasmin D. Tran, Anthony E. Bishay, Eduardo Monarrez, Richard E. Hartman, Maximillian E. Denys, Valeria Carrillo, Syed A. Uddin, Karl-Werner Schramm, Gregory Lampel, Julia M. Krum, Bernhard Henkelmann, Elena V. Kozlova, Prasada Rao S. Kodavanti, Margarita C. Currás-Collazo, Allison L. Phillips, Duraan S. Olomi, Nicole M. Huffman, Matthew Valdez, Brigitte M. Vazquez, Laura M. Anchondo, Heather M. Stapleton, Gladys Chompre, Bhuvaneswari D. Chinthirla, Kayhon M. Rabbani, Gwendolyn Gonzalez
Jazyk: angličtina
Rok vydání: 2021
Předmět:
medicine.medical_specialty
Vasopressin
Pediatric Research Initiative
Offspring
Health
Toxicology and Mutagenesis
Intellectual and Developmental Disabilities (IDD)
Autism
Neuropeptide
Biology
Toxicology
Developmental exposure
Oxytocin
Basic Behavioral and Social Science
Flame retardants
Supraoptic nucleus
Mice
Neurochemical
Internal medicine
Behavioral and Social Science
medicine
Polybrominated diphenyl ethers
Halogenated Diphenyl Ethers
Animals
Humans
Autistic Disorder
reproductive and urinary physiology
Pediatric
Endocrine-disrupting chemicals
Neuropeptides
Neurosciences
General Medicine
Pharmacology and Pharmaceutical Sciences
Reproductive Toxicology
Oxytocin receptor
Developmental Exposure
Endocrine-disrupting Chemicals
Flame Retardants
Polybrominated Diphenyl Ethers
Brain Disorders
Mice
Inbred C57BL
Stria terminalis
Endocrinology
Mental Health
Phenotype
Maternal Exposure
Female
medicine.drug
Zdroj: Archives of Toxicology
Arch. Toxicol., DOI: 10.1007/s00204-021-03163-4 (2021)
ISSN: 1432-0738
0340-5761
Popis: 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.
Databáze: OpenAIRE
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