Regular ArticleAcute Exposure to Methylmercury Opens the Mitochondrial Permeability Transition Pore in Rat Cerebellar Granule Cells☆
References (61)
- et al.
Calcineurin and mitochondrial function in glutamate-induced neuronal cell death
FEBS Lett.
(1996) - et al.
Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations
J. Biol. Chem.
(1992) - et al.
Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore. I. Evidence for two separate Me2+ binding sites with opposing effects on the pore open probability
J. Biol. Chem.
(1993) Calbindin D-28k and parvalbumin in the rat nervous system
Neuroscience
(1990)- et al.
Electron microscopic histochemical study on the localization and distribution of mercury in the nervous system after mercury intoxication
Exp. Neurol.
(1972) - et al.
Methylmercury alters intrasynaptosomal concentrations of endogenous polyvalent cations
Toxicol. Appl. Pharmacol.
(1993) - et al.
Simultaneous imaging of cell and mitochondrial membrane potentials
Biophys. J.
(1989) - et al.
Mercuric compounds inhibit human monocyte function by inducing apoptosis: Evidence for formation of reactive oxygen species, development of mitochondrial membrane permeability transition and loss of reductive reserve
Toxicology
(1997) Depression of frog muscle contraction by methylmercuric chloride and mercuric chloride
Toxicol. Appl. Pharmacol.
(1976)- et al.
Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms
Toxicol. Appl. Pharmacol.
(1987)
Ca2+ acting at the external side of the inner mitochondrial membrane can stimulate mitochondrial permeability transition induced by phenylarsine oxide
Biochim. Biophys. Acta
Methylmercury induces apoptosis of rat cerebellar neurons in primary culture
Biochem. Biophys. Res. Commun.
Organometal-induced increases in oxygen reactive species: The potential of 2′,7′-dichlorofluorescin diacetate as an index of neurotoxic damage
Toxicol. Appl. Pharmacol.
Inhibition of mitochondrial Ca2+ release diminishes the effectiveness of methyl mercury to release acetylcholine from synaptosomes
Toxicol. Appl. Pharmacol.
Pathways mediating Ca2+ entry in rat cerebellar granule cells following in vitro exposure to methyl mercury
Toxicol. Appl. Pharmacol.
Elevations of intracellular Ca2+ as a probable contributor to decreased viability in cerebellar granule cells following acute exposure to methylmercury
Toxicol. Appl. Pharmacol.
Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore. II. The minimal requirements for pore induction underscore a key role for transmembrane electrical potential, matrix pH, and matrix Ca2+
J. Biol. Chem.
Oxidative mechanisms underlying methyl mercury neurotoxicity
Int. J. Dev. Neurosci.
On the voltage dependence of the mitochondrial permeability transition pore. A critical appraisal
J. Biol. Chem.
Low-level methylmercury exposure causes human T-cells to undergo apoptosis: Evidence of mitochondrial dysfunction
Environ. Res.
Role of mitochondrial Ca2+ regulation in neuronal and glial cell signalling
Brain Res. Brain Res. Rev.
Role of the mitochondrial permeability transition in salicylate toxicity to cultured rat hepatocytes: Implications for the pathogenesis of Reye's syndrome
Toxicol. Appl. Pharmacol.
Irreversible suppression of calcium entry into nerve terminals by methylmercury
J. Pharmacol. Exp. Ther.
Methylmercury-induced depression of neuromuscular transmission in the rat
Neurotoxicology
Methylmercury poisoning in Iraq
Science
The permeability transition pore as a mitochondrial calcium release channel: A critical appraisal
J. Bioenerg. Biomembr.
A reevaluation of the role of mitochondria in neuronal Ca2+ homeostasis
J. Neurochem.
Mercury
Methylmercury-induced elevations in intrasynaptosomal zinc concentrations: An 19F-NMR study
J. Neurochem.
Intracellular calcium concentrations during “chemical hypoxia” and excitotoxic neuronal injury
J. Neurosci.
Cited by (82)
Neurotoxicity of mercury: An old issue with contemporary significance
2021, Advances in NeurotoxicologyAMPA receptor contribution to methylmercury-mediated alteration of intracellular Ca<sup>2+</sup> concentration in human induced pluripotent stem cell motor neurons
2020, NeuroToxicologyCitation Excerpt :In the second phase, there was a significant difference between the 0.1 μM and all other concentrations as well as 0.5 μM MeHg compared to all other concentrations (Fig. 9B). Increasing the concentration of MeHg does not reliably alter the extent of fura-2 fluorescence, but does hasten the onset of the effects (Hare et al., 1993; Marty and Atchison, 1997; Limke and Atchison, 2002; Ramanathan and Atchison, 2011). The AMPA/KA receptor antagonist CNQX was used to identify if AMPARs contributed to the observed increases in fura-2 fluorescence in hiPSC-MNs in response to MeHg.
Plant components can reduce methylmercury toxication: A mini-review
2019, Biochimica et Biophysica Acta - General SubjectsPost-translational modifications in MeHg-induced neurotoxicity
2019, Biochimica et Biophysica Acta - Molecular Basis of DiseaseBiomarkers of Oxidative/Nitrosative Stress and Neurotoxicity
2019, Biomarkers in ToxicologyEffects of methylmercury and retinol palmitate co-administration in rats during pregnancy and breastfeeding: Metabolic and redox parameters in dams and their offspring
2018, Ecotoxicology and Environmental Safety
- ☆
Supported by NIEHS Grant ES03299. T. L. Limke (née Stringfellow) was supported by NIEHS Grant T32-ES07255. Submitted in partial fulfillment of the requirement for the Degree of Doctor of Philosophy (T.L.). Portions of this study were presented in abstract form (Soc. Neurosci. Abstr.24, 1080, 1998; Toxicologist48, 241, 1999).
- 2
To whom correspondence and reprint requests should be addressed at Michigan State University, Dept. Pharmacology/Toxicology, B331 Life Sciences, East Lansing, MI 48824-1317. Fax: (517) 353-8915; E-mail: [email protected].