Brian M. Cox
EducationPh.D. in Pharmacology, St. Mary's Hospital Medical School, University of London, London, United Kingdom, 1965
B.Sc. in Pharmacolopy, Chelsea College of Science & Technology, University of London, London, United Kingdom, 1962
BiographyDr. Cox is currently Professor of Pharmacology and Neuroscience at the Uniformed Services University (USU) in Bethesda MD. He received his initial training in pharmacology from Chelsea College of Science and Technology in London, UK, and received a Ph.D. in Pharmacology from St. Mary's Hospital Medical School, University of London, UK. After teaching pharmacology to pharmacy and science students at Chelsea College of Science and Technology of the University of London for eight years, he became a visiting scientist in the Department of Pharmacology at Stanford University, and was appointed Consulting Associate Professor of Pharmacology at Stanford in 1978. Concurrently, he served as Laboratory Research Group Director and then Associate Director for Research for the Addiction Research Foundation in Palo Alto, CA. In 1981, Dr. Cox moved to his current position at USU, where he served as chair of the Department of Pharmacology from 1995 until 2007. He currently also serves as an Assistant Dean for Graduate Education at USU.
For most of his career Dr. Cox's research has focused on characterizing the receptors utilized by opiate drugs and their endogenous ligands, and in defining potential physiological and pathophysiological roles for endogenous opioids and other neuropeptides. His lab is currently studying factors affecting peptide and receptor expression, and changes at the cellular level induced by drugs of abuse, severe stress, or neural injury. He now leads the Biomarkers Group of the USU/NIH Center for Neuroscience and Regenerative Medicine, evaluating neurochemical mechanisms underlying traumatic brain injury and potential biomarkers for TBI.
Dr. Cox has been a member of the American Society for Pharmacology and Experimental Therapeutics (ASPET) since 1976. He served as Secretary/Treasurer of (1997-2000), and was elected President of ASPET for 2009-2010. He chaired the ASPET Board of Publications Trustees from 2002-2007. He has served on the Editorial Boards of the Journal of Pharmacology and Experimental Therapeutics (1998 – present), Molecular Pharmacology (1981-1994), and Molecular Interventions (2000-2002). Dr. Cox was a member of the ASPET Scientific Program Committee from 1986-1990 and Chaired the Program Committee from 1990-1996. He served as ASPET’s representative to the Experimental Biology Program Committee from 1991-1994 and served on the Experimental Biology Board from 1996-1999 (as Chairman for 1998-1999). He is currently serving a second term as a member of the Board of Directors of the Federation of American Societies of Experimental Biology.
Dr. Cox was the ASPET representative to the International Advisory Committee for the 1998 International Union of Pharmacology (IUPHAR) Congress in Munich, Germany, and chaired the IUPHAR World Congress of Pharmacology Scientific Program Committee for the 2002 meeting, held in San Francisco, CA. He is also a member of the British Pharmacological Society, the Society for Neuroscience, the AAAS, the American Society for Neurochemistry, and the International Narcotics Research Conference (for which he served as President from 1994-1998).
Representative publications, projects, and/or deployments
Assistant Dean for Graduate Education, Uniformed Services University, Bethesda MD 20814, since 2014
Director, Biospecimen Repository, Center for Neuroscience & Regenerative Medicine, Uniformed Services University, Bethesda MD 20814, since 2009
Professor of Pharmacology, Uniformed Services University, Bethesda MD 20814, since 1981
Associate Director for Research, Addiction Research Foundation, Stanford, California, 94305, 1977-1981
Consulting Associate Professor of Pharmacology, Stanford University, Stanford CA, 94305. 1978 - 1981
Research Associate, Director, Laboratory Research Group, Addiction Research Foundation, Stanford, California, 94305, 1973-1977
Lecturer (British System) in Pharmacology, Chelsea College, University of London, London, United Kingdom, 1965-1973
Nicholas Research Fellow, St. Mary's Hospital Medical School, University of London, London, United Kingdom, 1962-1965
Cox, B.M. and Weinstock, M. Quantitative studies of the antagonism by nalorphine of some of the actions of morphine-like analgesic drugs. Br. J. Pharmac. 22:289-300, 1964.
Cox, B.M. and Osman, O.H. Inhibition of the development of tolerance to morphine in rats by drugs which inhibit ribonucleic acid or protein synthesis. Br. J. Pharmac. 38:157-170, 1970.
Cox, B.M., Opheim, K., Teschemacher, H.-J. and Goldstein, A. A peptide-like substance from pituitary that acts like morphine. 2. Purification and properties. Life Sci. 16:1777-1782, 1975.
Goldstein, A., Cox, B.M., Klee, W.A., and Nirenberg, M. Endorphin from pituitary inhibits cyclic AMP formation in homogenates of neuroblastoma X glioma hybrid cells. Nature 265:362-363, 1977.
Whitnall, M.H., Gainer, H., Cox, B.M. and Molineaux, C.J. Dynorphin A(1-8) is contained within vasopressin neurosecretory vasicles in rat pituitary. Science 222:1137-1139, 1983.
Faden, A.I., Molineaux, C.J., Rosenberger, J.G., Jacobs, T.P. and Cox, B.M. Endogenous opioid immunoreactivity in rat spinal cord following traumatic injury. Ann. Neurol. 17:386-390, 1985.
Werling, L.L., Puttfarcken, P.S. and Cox, B.M. Multiple agonist-affinity states of opioid receptors: regulation of binding by guanyl nucleotides in guinea pig cortical, NG108-15, and 7315c cell membranes. Mol. Pharmacol. 33:423-431, 1988.
Marti M, Mela F, Fantin M, Zucchini S, Brown JM, Witta J, Di Benedetto M, Buzas B, Reinscheid RK, Salvadori S, Guerrini R, Romualdi P, Candeletti S, Simonato M, Cox BM and Morari M. Blockade of nociceptin/orphanin FQ transmission attenuates symptoms and neurodegeneration associated with Parkinson’s disease. J. Neuroscience 25: 9591-9601, 2005.
Authement ME, Kodangatil JN, Gouty S, Rusnak M, Symes AJ, Cox BM, Nugent F. Histone deacetylase inhibition rescues maternal deprivation-induced GABAergic metaplasticity through restoration of AKAP signaling. Neuron 86: 1240-1252, 2015.
Authement M, Kassis H, Langlois L, Gouty S, Dacher M, Sheopard R, Cox BM & Nugent FS. Morphine-induced synaptic abnormalities in the VTA are reversed by HDAC inhibition. J. Neurophysiol. 116(3): 1093-1103, 2016.