Methamphetamine (METH) is an addictive stimulant drug that acts on certain systems in the brain and can induce loss of function in neurons. Acute exposure to METH increases the release and blocks the reuptake of the neurotransmitter dopamine (DA), a biochemical messenger involved in many processes, including reward, motivation, and motor function. This can result in high levels of DA availability in the brain and can affect areas involved in dopaminergic transmission, such as the substantia nigra. Degeneration of dopaminergic neurons in this region of the brain has been highly implicated in the neurodegenerative disorder, Parkinson’s Disease. Based on our lab’s past research, METH has been shown to be neurotoxic to hippocampal neurons and can lead to cell death in specific sub-regions including the dentate gyrus up to 8 weeks after administration. Our present hypothesis is that a bolus dose of METH (30 mg/kg) in mice will also provoke continued cell loss within the substantia nigra pars compacta. Using immunohistochemistry techniques, including the fluorescent marker of neurodegeneration Fluoro-Jade C, we will examine various cell layers of the substantia nigra for dopaminergic cell death. Cell loss within the substantia nigra may indicate that a single bolus dose of METH may have similar neurodegenerative consequences seen in Parkinson’s Disease.