Pathways mediating Ca2+ entry in rat cerebellar granule cells following in vitro exposure to methyl mercury

Toxicology and Applied Pharmacology
M S Marty, William D Atchison

Abstract

Cell imaging and the Ca(2+)-sensitive fluorophore fura-2 were used to examine methyl mercury's effect on Ca2+ homeostasis in rat cerebellar granule cells, a cell type preferentially targeted by methyl mercury. In vitro methyl mercury exposure (0.2-5.0 microM) induced a biphasic rise in fura-2 fluorescence ratio, consisting of a small first phase due to Ca2+ release from intracellular store(s) and a much larger second phase which required Ca2+ influx. The time-to-onset of these fura-2 fluorescence changes was inversely correlated with methyl mercury concentration. When examining various Ca2+ entry pathways as possible targets contributing to Ca2+ influx, we found that excitatory amino acid pathways were not directly involved. In contrast, the voltage-dependent Ca2+ channel blockers nifedipine and omega-conotoxin-MVIIC significantly delayed the time-to-onset of both phases, a response inconsistent with mere inhibition of Ca2+ entry. The nonselective voltage-dependent Ca2+ channel blocker Ni2+ had no effect on the methyl mercury response. Because methyl mercury alters cell membrane potentials, we hypothesized that voltage-dependent Na+ channels were activated initially; however, tetrodotoxin did not alter the methyl mercury-induce...Continue Reading

Citations

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