ArticleDevelopmental neurobiology2013
Neural stem cell apoptosis after low-methylmercury exposures in postnatal hippocampus produce persistent cell loss and adolescent memory deficits.
Article in Developmental neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Developmental exposure to legacy environmental contaminants, medial temporal lobe volumes and spatial navigation memory in late adolescents.Environmental research · 2025Article
- The Preventive Effects of Salubrinal against Pyrethroid-Induced Disruption of Adult Hippocampal Neurogenesis in Mice.International journal of molecular sciences · 2023Article
- Prenatal low-dose methylmercury exposure causes premature neuronal differentiation and autism-like behaviors in a rodent model.iScience · 2023Article
- Associations between developmental exposure to environmental contaminants and spatial navigation in late adolescence.New directions for child and adolescent development · 2022Article
- Necrotic-like BV-2 microglial cell death due to methylmercury exposure.Frontiers in pharmacology · 2022Article
- Heavy metals and adult neurogenesis.Current opinion in toxicology · 2021Article
- Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation.International journal of molecular sciences · 2021Review
- Deltamethrin Exposure Inhibits Adult Hippocampal Neurogenesis and Causes Deficits in Learning and Memory in Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Methylmercury Impact on Adult Neurogenesis: Is the Worst Yet to Come From Recent Brazilian Environmental Disasters?Frontiers in aging neuroscience · 2020Article
- Methylmercury Interactions With Gut Microbiota and Potential Modulation of Neurogenic Niches in the Brain.Frontiers in neuroscience · 2020Article
- Leaf extracts from Dendropanax morbifera Léveille mitigate mercury-induced reduction of spatial memory, as well as cell proliferation, and neuroblast differentiation in rat dentate gyrus.BMC complementary and alternative medicine · 2019Article
- 17β-Estradiol Treatment Attenuates Neurogenesis Damage and Improves Behavior Performance After Ketamine Exposure in Neonatal Rats.Frontiers in cellular neuroscience · 2019Article
- The Putative Role of Environmental Mercury in the Pathogenesis and Pathophysiology of Autism Spectrum Disorders and Subtypes.Molecular neurobiology · 2018Review
- MeHg Causes Ultrastructural Changes in Mitochondria and Autophagy in the Spinal Cord Cells of Chicken Embryo.Journal of toxicology · 2018Article
- Aerobic Fitness and Neurocognitive Function Scores in Young Faroese Adults and Potential Modification by Prenatal Methylmercury Exposure.Environmental health perspectives · 2017Article
- Low-Dose Methylmercury-Induced Genes Regulate Mitochondrial Biogenesis via miR-25 in Immortalized Human Embryonic Neural Progenitor Cells.International journal of molecular sciences · 2016Article
- Methylmercury and brain development: A review of recent literature.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2016Review
- Effect ofExperimental and therapeutic medicine · 2016Article
- Early Developmental Low-Dose Methylmercury Exposure Alters Learning and Memory in Periadolescent but Not Young Adult Rats.BioMed research international · 2016Article
- Is Low Non-Lethal Concentration of Methylmercury Really Safe? A Report on Genotoxicity with Delayed Cell Proliferation.PloS one · 2016Article
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6 authors.
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Abstract
The developing brain is particularly sensitive to exposures to environmental contaminants. In contrast to the adult, the developing brain contains large numbers of dividing neuronal precursors, suggesting that they may be vulnerable targets. The postnatal day 7 (P7) rat hippocampus has populations of both mature neurons in the CA1-3 region as well as neural stem cells (NSC) in the dentate gyrus (DG) hilus, which actively produce new neurons that migrate to the granule cell layer (GCL). Using this well-characterized NSC population, we examined the impact of low levels of methylmercury (MeHg) on proliferation, neurogenesis, and subsequent adolescent learning and memory behavior. Assessing a range of exposures, we found that a single subcutaneous injection of 0.6 µg/g MeHg in P7 rats induced caspase activation in proliferating NSC of the hilus and GCL. This acute NSC death had lasting impact on the DG at P21, reducing cell numbers in the hilus by 22% and the GCL by 27%, as well as reductions in neural precursor proliferation by 25%. In contrast, non-proliferative CA1-3 pyramidal neuron cell number was unchanged. Furthermore, animals exposed to P7 MeHg exhibited an adolescent spatial memory deficit as assessed by Morris water maze. These results suggest that environmentally relevant levels of MeHg exposure may decrease NSC populations and, despite ongoing neurogenesis, the brain may not restore the hippocampal cell deficits, which may contribute to hippocampal-dependent memory deficits during adolescence.
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