Month/Year of Graduation
5-2024
Degree Name
Bachelor of Science (B.S.)
Department
Neuroscience
First Advisor
Dr. Ernest Chivero
Abstract
Methamphetamine (meth) use continues to increase in the United States despite the apparent health risks that involve neuroinflammation and brain damage. Because neuroinflammation underlies several substance-use and neurological disorders, we investigated whether microglia, the resident immune cells in the brain, are activated and consequently increase production of pro-inflammatory chemokines such as C- C chemokine ligand 2 (CCL2) in the presence of increasing amounts of meth. To address this, we exposed immortalized microglia cells (IMG) isolated from mature mouse brains to increasing concentrations of meth (0, 10, 50, 100, 500 µM) and analyzed for the expression levels of activation markers (CD11b and TMEM119) and the pro-inflammatory marker (CCL2) by Western blotting. Results show that exposure of IMG microglia to meth led to a dose dependent increase in the expression of CD11b, TMEM119 and CCL2. These results demonstrate that microglia become activated in a dose-dependent manner when exposed to meth. These results suggest that methamphetamine-induced brain damage may involve inflammation and pro-inflammatory chemokines and cytokines released by activated microglia.
Recommended Citation
Bredenkamp, Colton, "Methamphetamine Activates Microglia and Increases Production of Pro-Inflammatory Chemokine C-C Ligand 2" (2024). Theses/Capstones/Creative Projects. 313.
https://digitalcommons.unomaha.edu/university_honors_program/313
Included in
Chemicals and Drugs Commons, Mental and Social Health Commons, Psychological Phenomena and Processes Commons