Document Type

Student Research Paper

Date

Fall 2017

Academic Department

Chemistry and Biochemistry

Faculty Advisor(s)

Dr. Tom Hagan

Abstract

Dopamine is the primary neurotransmitter associated with addiction. Among the drugs that impact dopamine function, cocaine notably causes long-term blunting of dopamine release. The “blunted-dopamine hypothesis” explains the behaviors of addiction via cocaine’s blunting effects. In a non-addicted brain, dopamine acts in the midbrain reward system to regulate pleasure and related emotions. The brain responds to rewarding stimuli by mobilizing dopaminergic neurons to release dopamine, causing the pleasure associated with eating, gambling, and drug use. Notable structures involved in dopamine pathways are the dorsal and ventral striata, the nucleus accumbens (a part of the ventral striatum), and the ventral tegmental area, where high concentrations of dopamine receptors are located. Though different dopamine receptor types impact addiction in different ways, D1 receptors are most involved in cocaine addiction. Amphetamine and other stimulants directly cause the brain to release dopamine. By increasing the rate at which neurons generate action potentials and the intensity of the action potentials generated, amphetamine significantly increases dopamine levels in the striatum. Amphetamine is therefore highly useful in the field of dopamine research, as researchers can directly induce dopamine release with their application. Cocaine also increases dopamine levels within the striatum by inhibiting the dopamine active transporter, the protein that removes dopamine from the synaptic cleft after it has been released. Dopamine levels are therefore greater following a cocaine-mediated dopamine release. These changes to dopamine function over time facilitate the changes to neurobiochemistry that promote cocaine addiction.

Notes

FYS 100 HC - co-winner of 2018 Anna Carper Excellence in Library Research Award

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