Parkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive and selective loss of dopaminergic neurons in the substantia nigra pars compacta (SNc). All cells use calcium (Ca²⁺), among other ions, to produce signals that regulate cell function. Ca²⁺ signals in neurons alter electrical activity and stimulate release of neurotransmitters. One of the roles of mitochondria is to help maintain adequate concentrations of Ca²⁺ within the cell.  The mitochondrial calcium uniporter (MCU) allows Ca²⁺ into the mitochondria matrix. Under stress conditions, more cytosolic Ca²⁺ is present in the cell, promoting excessive Ca²⁺ uptake by the MCU. It is thought that this excess mitochondrial Ca²⁺ uptake may promote Parkinson’s disease. A mechanism that regulates mitochondrial Ca²⁺ uptake in dopaminergic cells would reveal a new target for therapeutic strategies to halt the progressive degeneration of SNc neurons in PD. One such mechanism would be to inhibit MCU and test if it protects from high levels of cytosolic Ca²⁺. We used SH-SY5Y cells treated with the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA). For this experiment, we inhibited the activity of the MCU by expressing a dominant-negative (DN) variant, restricting Ca²⁺ uptake into the mitochondria matrix. We found that the expression of DN-MCU does not reduce cell death, and in some may even promote cell death.  The expression of DN-MCU may generate persistent excessive levels of cytosolic Ca²⁺, generating stress conditions that ultimately leads to cell death.