Title

The Effects of Adolescent Methylphenidate Exposure on the Expression of ΔFosB in the Prefrontal Cortex and Striatum

Faculty Mentor(s)

Dr. Ryan Shanks; Dr. Steven Lloyd

Campus

Dahlonega

Subject Area

Biology

Location

Library Room 269:Open Classroom

Start Date

31-3-2014 12:00 PM

End Date

31-3-2014 1:30 PM

Description/Abstract

Methylphenidate (MPD), the active ingredient in Ritalin®, is a psychostimulant whose main mechanism of action is to block dopamine transporters. MPD abuse is on the rise amongst adolescents given its euphoric and nootropic effects. Chronic drug abuse is known to have lasting effects on neural plasticity. Multiple studies with other stimulants indicate accumulation of the transcription factor ΔFosB in areas of the brain associated with reward and compulsivity, leading to speculations on the protein’s role in drug addiction and relapse. Previous behavioral research in our lab demonstrated MPD-induced behavioral changes in both prenatal and adolescent exposure paradigms. In this study, we investigated the same MPD-exposure dosing paradigms. The prefrontal cortex and striatum for each mouse were micro-dissected, homogenized, and total RNA was isolated. Drug induced changes in fosB expression will be measured using qPCR against experimental and internal controls (i.e., 18S). We hypothesize that there will be increased expression of the fosB gene in mice treated with methylphenidate compared to those treated with saline in both exposure paradigms. Through an understanding of the physical mechanisms by which chronic drug abuse alters the brain, we can seek therapeutic methods that will target and treat the drug-induced damage.

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Mar 31st, 12:00 PM Mar 31st, 1:30 PM

The Effects of Adolescent Methylphenidate Exposure on the Expression of ΔFosB in the Prefrontal Cortex and Striatum

Library Room 269:Open Classroom

Methylphenidate (MPD), the active ingredient in Ritalin®, is a psychostimulant whose main mechanism of action is to block dopamine transporters. MPD abuse is on the rise amongst adolescents given its euphoric and nootropic effects. Chronic drug abuse is known to have lasting effects on neural plasticity. Multiple studies with other stimulants indicate accumulation of the transcription factor ΔFosB in areas of the brain associated with reward and compulsivity, leading to speculations on the protein’s role in drug addiction and relapse. Previous behavioral research in our lab demonstrated MPD-induced behavioral changes in both prenatal and adolescent exposure paradigms. In this study, we investigated the same MPD-exposure dosing paradigms. The prefrontal cortex and striatum for each mouse were micro-dissected, homogenized, and total RNA was isolated. Drug induced changes in fosB expression will be measured using qPCR against experimental and internal controls (i.e., 18S). We hypothesize that there will be increased expression of the fosB gene in mice treated with methylphenidate compared to those treated with saline in both exposure paradigms. Through an understanding of the physical mechanisms by which chronic drug abuse alters the brain, we can seek therapeutic methods that will target and treat the drug-induced damage.