ArticleToxicological sciences : an official journal of the Society of Toxicology2023
Aryl hydrocarbon receptor activation affects nitrergic neuronal survival and delays intestinal motility in mice.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- Interaction of the Gut Microbiota and the Enteric Nervous System: Implications in Gastrointestinal Disorders Associated With Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2026Review
- Aryl hydrocarbon receptor deficiency leads to sex- and age-dependent colonic dysmotility in mice.Journal of physiology and biochemistry · 2026Article
- CYP1A1 as a conserved metabolic circuit linking environmental sensing to immune regulation.Archives of toxicology · 2026Review
- Tryptophan metabolism in glaucomatous optic neuropathy: from metabolic dysregulation to therapeutic opportunities.Journal of translational medicine · 2026Review
- Modulation of Ceramide-Induced Apoptosis in Enteric Neurons by Aryl Hydrocarbon Receptor Signaling: Unveiling a New Pathway beyond ER Stress.International journal of molecular sciences · 2024Article
- Risk of Dementia in Korean Vietnam War Veterans.The journal of prevention of Alzheimer's disease · 2024Article
- Activation of the aryl hydrocarbon receptor in inflammatory bowel disease: insights from gut microbiota.Frontiers in cellular and infection microbiology · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Despite progress describing the effects of persistent organic pollutants (POPs) on the central nervous system, the effect of POPs on enteric nervous system (ENS) function remains underexplored. We studied the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a POP, and a potent aryl hydrocarbon receptor (AHR) ligand, on the ENS and intestinal motility in mice. C57Bl/6J mice treated with TCDD (2.4 µg/kg body weight) for 8 weeks (once per week) exhibited significant delay in intestinal motility as shown by reduced stool frequency, prolonged intestinal transit time, and a persistence of dye in the jejunum compared to control mice with maximal dye retention in the ileum. TCDD significantly increased Cyp1a1 expression, an AHR target gene, and reduced the total number of neurons and affected nitrergic neurons in cells isolated from WT mice, but not Ahr-/- mice. In immortalized fetal enteric neuronal cells, TCDD-induced nuclear translocation of AHR as well as increased Cyp1a1 expression. AHR activation did not affect neuronal proliferation. However, AHR activation resulted in enteric neuronal toxicity, specifically, nitrergic neurons. Our results demonstrate that TCDD adversely affects nitrergic neurons and thereby contributes to delayed intestinal motility. These findings suggest that AHR signaling in the ENS may play a role in modulating TCDD-induced gastrointestinal pathophysiology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.