ArticleToxicology and applied pharmacology2011
Gestational lead exposure selectively decreases retinal dopamine amacrine cells and dopamine content in adult mice.
Article in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Retinal toxicity of heavy metals and its involvement in retinal pathology.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2024Review
- Evidence of Synaptic and Neurochemical Remodeling in the Retina of Aging Degus.Frontiers in neuroscience · 2020Article
- Alpha lipoic acid attenuates the long-term effects of lead exposure in retinal ischemic injury mouse model.Environmental science and pollution research international · 2019Article
- Brs3 neurons in the mouse dorsomedial hypothalamus regulate body temperature, energy expenditure, and heart rate, but not food intake.Nature neuroscience · 2018Article
- Metals and Circadian Rhythms.Advances in neurotoxicology · 2017Article
- Increased proliferation of late-born retinal progenitor cells by gestational lead exposure delays rod and bipolar cell differentiation.Molecular vision · 2016Article
- Mitochondrial complex I deficiency leads to inflammation and retinal ganglion cell death in the Ndufs4 mouse.Human molecular genetics · 2015Article
- Article
- Developmental origins of adult diseases and neurotoxicity: epidemiological and experimental studies.Neurotoxicology · 2012Article
- Bcl-xL-mediated remodeling of rod and cone synaptic mitochondria after postnatal lead exposure: electron microscopy, tomography and oxygen consumption.Molecular vision · 2012Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Gestational lead exposure (GLE) produces supernormal scotopic electroretinograms (ERG) in children, monkeys and rats, and a novel retinal phenotype characterized by an increased number of rod photoreceptors and bipolar cells in adult mice and rats. Since the loss of dopaminergic amacrine cells (DA ACs) in GLE monkeys and rats contributes to supernormal ERGs, the retinal DA system was analyzed in mice following GLE. C57BL/6 female mice were exposed to low (27 ppm), moderate (55 ppm) or high (109 ppm) lead throughout gestation and until postnatal day 10 (PN10). Blood [Pb] in control, low-, moderate- and high-dose GLE was ≤ 1, ≤ 10, ~25 and ~40 μg/dL, respectively, on PN10 and by PN30 all were ≤ 1 μg/dL. At PN60, confocal-stereology studies used vertical sections and wholemounts to characterize tyrosine hydroxylase (TH) expression and the number of DA and other ACs. GLE dose-dependently and selectively decreased the number of TH-immunoreactive (IR) DA ACs and their synaptic plexus without affecting GABAergic, glycinergic or cholinergic ACs. Immunoblots and confocal revealed dose-dependent decreases in retinal TH protein expression and content, although monoamine oxidase-A protein and gene expression were unchanged. High-pressure liquid chromatography showed that GLE dose-dependently decreased retinal DA content, its metabolites and DA utilization/release. The mechanism of DA selective vulnerability is unknown. However, a GLE-induced loss/dysfunction of DA ACs during development could increase the number of rods and bipolar cells since DA helps regulate neuronal proliferation, whereas during adulthood it could produce ERG supernormality as well as altered circadian rhythms, dark/light adaptation and spatial contrast sensitivity.
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