ABSTRACTand was abolished by mitochondrial depolarization. The secondary increase was associated with spreading of the dye from punctate staining to whole-cell distribution, and was delayed significantly by the MTP inhibitor cyclosporin A and the smooth endoplasmic reticulum Ca 2ϩ ATPase inhibitor thapsigargin. We conclude that MeHg causes release of Ca 2ϩ from the mitochondria through opening of the MTP, which contributes the bulk of the elevated [Ca 2ϩ ] i observed during MeHg neurotoxicity. Additionally, the Ca 2ϩ that enters the mitochondria seems to originate in the smooth endoplasmic reticulum, providing a mechanism for the observed mitochondrial Ca 2ϩ overload.

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