Date Approved


Embargo Period


Document Type


Degree Name

Master of Sciences in Pharmaceutical Sciences


Chemistry and Biochemistry


College of Science & Mathematics


James P. Grinias, Ph.D

Committee Member 1

James P. Grinias, Ph.D

Committee Member 2

David M. Devilbiss, Ph.D

Committee Member 3

Amos Mugweru, Ph.D


traumatic brain injury, neurotransmitters, catecholamine signaling, medial prefrontal cortex


Brain--Research; Catecholamines


Chemistry | Medicine and Health Sciences | Pharmacy and Pharmaceutical Sciences | Physical Sciences and Mathematics


Traumatic brain injury (TBI) is a serious global health burden that causes a wide range of neurocognitive symptoms. These cognitive processes are regulated by catecholamine signaling within the prefrontal cortex (PFC) region of the brain. To quantify functional deficits in catecholamine signaling after TBI, norepinephrine (NE) and dopamine (DA) levels within the PFC were quantified from microdialysate samples using high-performance liquid chromatography coupled with electrochemical detection. A method for benzoyl chloride derivatization of neurotransmitters and analysis with liquid chromatography and tandem mass spectrometry instrumentation was also developed to detect and analyze these neurotransmitters. Overall, it was found that catecholamine signaling is dysfunctional after TBI with significant reductions in PFC neurotransmission. Responsivity of NE and DA to a putative catecholamine based TBI therapy, methylphenidate (Ritalin®), was blunted. These results suggest that following TBI, there is a dysregulation of the catecholamine systems that likely contributes to cognitive deficits found after TBI.

Available for download on Saturday, May 31, 2025