Randall L. Davis, Ph.D.
Director, Biomedical Sciences Graduate Program
Associate Professor of Pharmacology
Texas Tech University
Oklahoma State University
B.S. (Biomedical Sciences)
Oklahoma State University
NRSA (NIAAA/NIH) Postdoctoral Fellow, Texas Tech University HSC (Pharmacology & Neuroscience).
Postdoctoral Research Associate, Texas Tech University HSC (Pharmacology)
NIH/NIAAA 4/01/2002 – 9/30/2004
NIH/NIAAA 5/01/2006 – 4/30/2008
NIH/NINDS 8/01/2008 – 6/30/2011 no-cost extension until 6/30/2012
OCAST 9/01/2014 – 8/31-2017
Davis RL, Buck D, Saffarian N, Stevens CW (2007) The opioid antagonist, β-funaltrexamine, inhibits chemokine expression in human astroglial cells. Journal of Neuroimmunology 186:141-149.
Sanchez AC, Davis RL, Syapin PJ (2007) The Oct DNA motif participates in the alcohol inhibition of the inducible nitric oxide synthase gene promoter in rat C6 glioma cells. Brain Research 1179:16-27.
Davis RL, Buck DJ, Saffarian N, Mohan S, Desilva U, Fernando SC, Stevens CW (2008) β-Funaltrexamine inhibits inducible nitric-oxide synthase expression in human astroglial cells. Journal of Neuroimmune Pharmacology 3:150-153.
Davis RL and Syapin PJ (2008) Importance of alcohol induced modulation of nitric-oxide synthase in the brain. In Research on the Neurobiology of Alcohol Use Disorders. (L. Sher, Ed.), Nova Science, New York.
Davis RL (2009) Central Nervous System Inflammation: Astroglia and Ethanol. In Encyclopedia of Neuroscience (M. Binder, N. Hirokawa, U. Windhorst, Eds.), Springer, New York, pp. 638-641.
Williams R, Dhillon NK, Hedge ST, Yao H, Callen S, Peng F, Chebloune Y, Davis RL, Buch SJ (2009) Pro-inflammatory cytokines and HIV-1 synergistically enhance CXCL10 expression in human astrocytes. Glia 57:734-743.
Mohan S, Davis RL, DeSilva U, Stevens CW (2010).Dual regulation of mu opioid receptors in SK-N-SH neuroblastoma cells by morphine and interleukin-1β: evidence for opioid-immune crosstalk. Journal of Neuroimmunology 227:26-34.
Saffarian N, Buck DJ, Zecca L, Davis RL (2010) Neuromelanin inhibits CXCL10 expression in human astroglial cells. Neuroscience Letters 486(1):47-50.
Curtis JT, Chen Y, Buck DJ, Davis RL (2011) Chronic inorganic mercury exposure induces sex-specific changes in central TNFα expression: Importance in autism?. Neuroscience Letters 504:40-44.
Assefa S, Curtis JT, Sethi S, Davis RL, Chen Y, Kaul R (2012) Inorganic mercury exposure in prairie vole (Microtus ochrogaster) alters the expression of toll-like receptor 4 and activates inflammatory pathways in the liver in a sex-specific manner. Human & Experimental Toxicology 31(4):376-386.
Tousi NS, Buck DJ, Curtis JT, Davis RL (2012) α-Synuclein potentiates interleukin-1β-induced CXCL10 expression in human A172 astrocytoma cells. Neuroscience Letters 507:133-136.
Stevens CW, Aravind S, Das S, Davis RL (2013) Pharmacological characterization of LPS and opioid interactions at the toll-like receptor 4. British Journal of Pharmacology 168:1421-1429.
Davis RL, Das S, Buck DJ, Stevens CW (2013) b-Funaltrexamine inhibits chemokine (CXCL10) expression in normal human astrocytes. Neurochemistry International 62:478-485.
Santos D, Batoreu MC, de Almeida IT, Davis RL, Mateus ML, Andrade V, Ramos R, Torres E, Aschner M, Marreilha dos Santos AP (2013) Evaluation of neurobehavioral and neuroinflammatory end-points in the post-exposure period in rats sub-acutely exposed to manganese. Toxicology 314(1), 95-99.
My research interests have always centered on neuroinflammation. Thus, our efforts are focused on understanding the neuroinflammatory events associated with CNS disorders such as Parkinson’s disease, HIV-dementia and mood/behavior disorders. We are particularly interested in inflammatory signaling in astrocytes and microglia and modulation of these signaling events by drugs of abuse and other pharmacologic agents. In our most recent investigations, we discovered that β-funaltrexamine (FNA), a selective, mu-opioid receptor (MOR) antagonist, has anti-inflammatory actions in vitro and in vivo. However, these anti-inflammatory actions are not related to classically defined actions through MOR. Our current efforts are therefore directed at identifying the mechanism of action for these anti-inflammatory effects of β-FNA in order to open a new line of inquiry into the potential of β-FNA (or modified forms of this compound) as an inhibitor of neuroinflammation to be included in combination drug treatment of neurologic diseases, in particular major depressive disorders.
My lab has expertise in cellular and molecular techniques used to assess neuroinflammatory signaling; including key techniques such as ELISA, transcription factor assays, immunoprecipitation, immunoblotting, immunohistochemistry, RT-PCR, ROS detection, cell culture, viability and apoptosis assays, and pharmacologic manipulations. In collaboration with several departmental colleagues, we also have experience with in vivo models of neuroinflammation, sickness behavior, depressive-like behavior and social withdrawal.
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