Title

The Effects of Methamphetamine on PRX Antioxidant Proteins in a Cultured Microglia Cell Line and a Mouse Model [Poster]

Faculty Mentor(s)

Steven Lloyd and Ryan Shanks

Proposal Type

Poster

Location

Library Technology Center 3rd Floor Open Area

Start Date

29-3-2012 4:30 PM

End Date

29-3-2012 6:30 PM

Description/Abstract

Abuse of the psychostimulant and dopamine (DA) agonist, methamphetamine (METH), leads to neurodegeneration of DAergic neurons in the striatum and prefrontal cortex. Previous data in our lab indicates DA neurons in the hypothalamus are not susceptible to METH-induced neurodegeneration. This studies focus is on the antioxidant mechanisms available to deal with the toxic free radicals created by METH induced oxidative stress. One such antioxidant, peroxiredoxin (PRX), represents a family of six antioxidant isoforms that reduces hydrogen peroxide, peroxynitrite, and organic hydroperoxides. We hypothesized that PRX expression would be increased and localized to the hypothalamus as a protective mechanism to METH exposure. Male C57B1/J6 mice were exposed to an abuse dosing paradigm of METH (n=5) or saline (n=5). Prefrontal cortex, striatum, and hypothalamus regions were collected and processed for PCR PRX mRNA expression analysis using isoform specific primers. There were no significant PRX mRNA expression changes in the prefrontal cortex or striatum. However, in the hypothalamus, there were significant METH-induced increases in PRX II, III, V, and VI. This study provides incite into the role PRX proteins in response to the dopaminergic damage associated with METH abuse, and has opened the door to further understanding into the protective mechanisms underlying neurodegeneration. [Poster]

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Mar 29th, 4:30 PM Mar 29th, 6:30 PM

The Effects of Methamphetamine on PRX Antioxidant Proteins in a Cultured Microglia Cell Line and a Mouse Model [Poster]

Library Technology Center 3rd Floor Open Area

Abuse of the psychostimulant and dopamine (DA) agonist, methamphetamine (METH), leads to neurodegeneration of DAergic neurons in the striatum and prefrontal cortex. Previous data in our lab indicates DA neurons in the hypothalamus are not susceptible to METH-induced neurodegeneration. This studies focus is on the antioxidant mechanisms available to deal with the toxic free radicals created by METH induced oxidative stress. One such antioxidant, peroxiredoxin (PRX), represents a family of six antioxidant isoforms that reduces hydrogen peroxide, peroxynitrite, and organic hydroperoxides. We hypothesized that PRX expression would be increased and localized to the hypothalamus as a protective mechanism to METH exposure. Male C57B1/J6 mice were exposed to an abuse dosing paradigm of METH (n=5) or saline (n=5). Prefrontal cortex, striatum, and hypothalamus regions were collected and processed for PCR PRX mRNA expression analysis using isoform specific primers. There were no significant PRX mRNA expression changes in the prefrontal cortex or striatum. However, in the hypothalamus, there were significant METH-induced increases in PRX II, III, V, and VI. This study provides incite into the role PRX proteins in response to the dopaminergic damage associated with METH abuse, and has opened the door to further understanding into the protective mechanisms underlying neurodegeneration. [Poster]