ArticleProceedings of the National Academy of Sciences of the United States of America2012
Rescue of neuronal migration deficits in a mouse model of fetal Minamata disease by increasing neuronal Ca2+ spike frequency.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 44 citations in OpenAlex.
- Effect of methylmercury on fetal neurobehavioral development: an overview of the possible mechanisms of toxicity and the neuroprotective effect of phytochemicals.Archives of toxicology · 2022Review
- Effect of alpha-mangostin in the prevention of behavioural and neurochemical defects in methylmercury-induced neurotoxicity in experimental rats.Toxicology reports · 2022Article
- Nrf2/HO-1 Signaling Activator Acetyl-11-keto-beta Boswellic Acid (AKBA)-Mediated Neuroprotection in Methyl Mercury-Induced Experimental Model of ALS.Neurochemical research · 2021Article
- The Role of Galanin in Cerebellar Granule Cell Migration in the Early Postnatal Mouse during Normal Development and after Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Prenatal Environment That Affects Neuronal Migration.Frontiers in cell and developmental biology · 2019Review
- Nasal Placode Development, GnRH Neuronal Migration and Kallmann Syndrome.Frontiers in cell and developmental biology · 2019Article
- Methylmercury alters proliferation, migration, and antioxidant capacity in human HTR8/SV-neo trophoblast cells.Reproductive toxicology (Elmsford, N.Y.) · 2018Article
- Gestational Age and Sex Influence the Susceptibility of Human Neural Progenitor Cells to Low Levels of MeHg.Neurotoxicity research · 2017Article
- Postnatal Migration of Cerebellar Interneurons.Brain sciences · 2017Review
- 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
- In Utero Bisphenol A Exposure Induces Abnormal Neuronal Migration in the Cerebral Cortex of Mice.Frontiers in endocrinology · 2016Article
- Ex vivo imaging of postnatal cerebellar granule cell migration using confocal macroscopy.Journal of visualized experiments : JoVE · 2015Article
- Control of cortical neuronal migration by glutamate and GABA.Frontiers in cellular neuroscience · 2015Review
- Calcium release-dependent actin flow in the leading process mediates axophilic migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Role of calcium and mitochondria in MeHg-mediated cytotoxicity.Journal of biomedicine & biotechnology · 2012Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
In the brains of patients with fetal Minamata disease (FMD), which is caused by exposure to methylmercury (MeHg) during development, many neurons are hypoplastic, ectopic, and disoriented, indicating disrupted migration, maturation, and growth. MeHg affects a myriad of signaling molecules, but little is known about which signals are primary targets for MeHg-induced deficits in neuronal development. In this study, using a mouse model of FMD, we examined how MeHg affects the migration of cerebellar granule cells during early postnatal development. The cerebellum is one of the most susceptible brain regions to MeHg exposure, and profound loss of cerebellar granule cells is detected in the brains of patients with FMD. We show that MeHg inhibits granule cell migration by reducing the frequency of somal Ca(2+) spikes through alterations in Ca(2+), cAMP, and insulin-like growth factor 1 (IGF1) signaling. First, MeHg slows the speed of granule cell migration in a dose-dependent manner, independent of the mode of migration. Second, MeHg reduces the frequency of spontaneous Ca(2+) spikes in granule cell somata in a dose-dependent manner. Third, a unique in vivo live-imaging system for cell migration reveals that reducing the inhibitory effects of MeHg on somal Ca(2+) spike frequency by stimulating internal Ca(2+) release and Ca(2+) influxes, inhibiting cAMP activity, or activating IGF1 receptors ameliorates the inhibitory effects of MeHg on granule cell migration. These results suggest that alteration of Ca(2+) spike frequency and Ca(2+), cAMP, and IGF1 signaling could be potential therapeutic targets for infants with MeHg intoxication.
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