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Journal of Undergraduate Research

Keywords

s-glutathionylation, VMAT, acute methamphetamine, dopaminergic neurons

College

Family, Home, and Social Sciences

Department

Psychology

Abstract

Methamphetamine (METH) has long been regarded as a potent addictive drug and psychostimulant. The addictive effects can be localized to the VTA, specifically activity of dopaminergic neurons in the nucleus accumbens (NAc). Overactivity of these neurons results in the pleasurable and addictive of METH. Various theories have been proposed as to the mechanism of this excess dopamine release; including a role for reactive oxygen species. In a recent publication, our lab has already demonstrated that METH induces the formation of reactive oxygen species (ROS) in the axon terminals of dopaminergic neurons in the nucleus accumbens and that blocking the formation of these ROS also attenuates METH’s effects on dopamine release. Using disulfiram as a controlled ROS, we have shown that oxidative stress significantly reduces the function of the vesicular monoamine transporter (VMAT) (Fig. 1). The purpose of the proposed experiment was to demonstrate the direct effects of METH on the VMAT2, particularly on reactive residues. We hypothesized that the ROS inhibit the function of the vesicular monoamine transporter 2 (VMAT2) by oxidizing the cysteine-488 residue.

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