B.S. Biochemistry, 2011
Kansas State University
Mentor: Dr. Michael F. Salvatore, PhD
Chotibut, T., Davis, R.W., Arnold, J.C., Frencheck, Z., Gurwara, S., Bondada, V., Geddes, J.W., Salvatore, M.F. 2013. Ceftriaxone increases glutamate uptake and reduces striatal tyrosine hydroxylase loss in 6-OHDA Parkinson’s model. Mol. Neurobiol. DOI 10.1007/s12035-013-8598-0.
Arndt, D.L., Arnold, J.C., Cain, M.E. 2013. Attenuation of amphetamine-induced hyperactivity and sensitization through glutamatergic alterations in enriched rats. Exp Clin Psychopharm, in press.
Salvatore, M.F., Chotibut, T., Arnold, J.C. “Dissecting Involvement of Glutamate Excitotoxicity in Parkinson’s disease” in Excitotoxicity: Fundamental concepts, Pathophysiology and Treatment Strategies. Metzger, E.D. & Halsey, K.G, Eds. Hauppauge, N.Y. USA: Nova Science Publishers, Inc., 2013. In press.
Salvatore, M.F, Davis, R.W., Arnold, J.C., Chotibut, T. 2012. Transient striatal GLT-1 blockade increases EAAC1 expression, glutamate reuptake, and decreases tyrosine hydroxylase phosphorylation at ser (19). Exp Neurol. 234(2): 428-36.
Gill, M.J., Arnold, J.C., Cain, M.E. 2011. Impact of mGluR5 during amphetamine-induced hyperactivity and conditioned hyperactivity in differentially reared rats. Psychopharmacology. 221(2): 227-37.
Academic & Professional Honors/Awards:
Brain Wellness Press Conference Speaker, Society for Neuroscience Conference, 2013
Shreveport Chapter of Society for Neuroscience Travel Award, 2013
1st Place Poster in Pre-Proposal Category, Graduate Research Day, LSU Health-Shreveport, 2012
Chapter Secretary, Shreveport Chapter of Society for Neuroscience, 2013-present
Graduate School Representative, LSU Health-Shreveport Library Committee, 2013-present
Graduate Student Distinguished Lecturer Committee, 2013-present
New Student Welcome Committee, 2014-present
Student Representative, Shreveport Chapter of Society for Neuroscience, 2012-2013
Research in our laboratory examines the molecular entities associated with locomotor function, with the goal of identifying therapeutic targets for locomotor impairments such as Parkinson’s disease and aging-related Parkinsonism
. We are particularly interested in the role that dopamine- and glutamate-regulating proteins have on the specific populations of neurons and glia that ultimately affect movement capabilities.
Bradykinesia, or the slowness of movement, is a major symptom of both Parkinson’s disease and aging. It is estimated that bradykinesia affects nearly 50% of the aging population by age 85. However, the cause of bradykinesia is not well understood, and consequently, there is no cure or drug available for treatment of bradykinesia. Thus, a major goal of our research is to determine the neurobiological basis of bradykinesia and develop strategies to prevent and/or mitigate its onset in aging.
There is evidence to show that physical exercise improves locomotor impairments associated with Parkinson’s disease, but few studies have determined if exercise has a similar impact on locomotor impairments in aging. Thus, one goal of my research is to utilize lifestyle strategies, like physical exercise, to prevent and/or mitigate age-related Parkinsonism. Through this work, we also will examine the underlying mechanism by which exercise improves locomotor capabilities. Importantly, these studies may highlight key therapeutic targets for drug development in the treatment of aging-related Parkinsonism, particularly for elderly patients who are unwilling or unable to participate in physical exercise.