Postdoctoral (Cell Biology & Neuroanatomy)
University of Minnesota
Ph.D. (Anatomy & Neurobiology)
University of Vermont
Kansas State University
Chair, Department Anatomy & Cell Biology, Oklahoma State University Center for Health Sciences (OSU-CHS), Tulsa, OK
Professor, Department Anatomy & Cell Biology, Oklahoma State University Center for Health Sciences (OSU-CHS), Tulsa, OK
Associate Professor, Department Anatomy & Cell Biology, Oklahoma State University Center for Health Sciences (OSU-CHS), Tulsa, OK
Assistant Professor, Department Cell Biology, University of Oklahoma Health Sciences Center (OUHSC), Oklahoma City, OK
Assistant Professor, Department of Anatomical Sciences, OUHSC
Group Leader, Analgesia Program, G.D. Searle & Co. Research & Development, Skokie, IL
Research Scientist, Neurotrophic Factors Program, G.D. Searle R&D, Monsanto CO and Chesterfield, MO
Research Assistant, Professor Department Neurol Surgery Miami Project to Cure Paralysis, Univeristy of Miami, Miami, FL
Postdoctoral Fellow, Department of Cell Biology and Neuroanatomy, University of Minnesota, Minneapolis, MN
Oklahoma State University Regents Distinguished Research Award
2006-present, 2003-2005, 1991-1993
Executive Committee, Oklahoma Center for Neuroscience
Experimental Biology Meeting Symposium organizer - “Glutamine and Glutamate Metabolism: Organ Specific Regulation”
Education Committee, Society for Neuroscience
President, Oklahoma Chapter, Society for Neuroscience
Papka, R.E., S. Williams, K.E. Miller, T. Copelin, and S. Puri, CNS location of uterine-related neurons revealed by transsynaptic tracing with pseudorabies virus & their relationship to estrogen-receptor immunoreactive neurons. Neuroscience 84:935-952, 1998.
Miller, K.E. and A.T. Salvatierra, Apposition of enkephalin- and neurotensin-immunoreactive neurons by serotonin-immunoreactive fibers in the rat spinal cord. Neuroscience, 85:837-846, 1998.
Miller, K.E., A.B. Richards, V.D. Douglas, M.J. Chandler, and R.D. Foreman, Propriospinal neurons in the rat C1-C2 segments project to the lower lumbar and sacral spinal cord. Brain Res. Bull. 47:43-47, 1998.
Komori, N., S.D. Cain, J.-M. Roch, K.E. Miller, and H. Matsumoto, Differential expression of alternative splice variants of B-arrestin-1 and –2 in rat central nervous system and peripheral tissues. Eur. J. Neurosci. 10:2607-2616, 1998.
Miller, K.E., E. Åkesson, and Å. Seiger, Nerve growth factor-induced stimulation of dorsal root ganglion/spinal cord co-grafts in oculo: Enhanced survival and growth of CGRP-immunoreactive sensory neurons. Cell Tiss.Res. 298:243-53, 1999.
Qin, C., M.J. Chandler, K.E. Miller, and R.D. Foreman, Chemical activation of cervical cell bodies: Effects on spontaneous activity and responses to colorectal distension in lumbosacral spinal cord of rats. J. Neurophysiol., 82:3423-33, 1999.
Benton, R.L., C.D. Ross, and K.E. Miller, Glutamine synthetase activities in spinal white and gray matter 7 days following spinal cord injury in rats. Neurosci. Lett. 291:1-4, 2000.
Gu, L., K.E. Miller, and G. Dryhurst, Dopaminergic neurotoxicity of L-cysteine after stereotaxic administration to rats: Implications for idiopathic and chemically-induced parkinosinism. Neurotoxicity Res. 2: 373-389, 2000.
Benton, R.L., C.D. Ross, and K.E. Miller, Spinal taurine levels are increased 7 and 30 days following methylprednisolone treatment of spinal cord injury in rats. Brain Res. 893:292-300, 2001.
Qin, C., M.J. Chandler, K.E. Miller, and R.D. Foreman, Responses and afferent pathways of superficial and deeper C1-C2 spinal neurons to pericadial administration of algogenic chemicals in rats. J Neurophysiol. 85(4):1522-1532, 2001.
Miller, K.E., B.A. Richards, and R.M. Kriebel, Glutamine-, glutamine synthetase-, glutamate dehydrogenase- and pyruvate carboxylase-immunoreactivities in the rat dorsal root ganglion and peripheral nerve. Brain Res. 945:202-11, 2002.
Qin, C., M.J. Chandler, K.E. Miller, and R.D. Foreman, Chemical activation of cardiac receptors affects activity of superficial and deeper T3-T4 spinal neurons in rats. Brain Res. 959:77-85, 2003.
Qin, C., M.J. Chandler, K. Miller, R.D. Foreman, Responses and afferent pathways of C1-C2 spinal neurons to gastric distension in rats. Autonomic Neurosci.: Basic and Clinical, 426:1-9, 2003 .
Komori, N., J. Neal, S.D. Cain, J. Logan, C. Wirsig, and K.E. Miller, Presence of β-Arrestin-1 in the cutaneous nerve fibers of rat hind paw. Brain Res. 988:121-129, 2003.
Schechter, R., D. Beju, and K.E. Miller, The effect of insulin deficiency in tau and neurofilament in the insulin knockout mouse. Biochem. Biophys. Res. Comm. 334:979-986, 2005.
Foster, S.B., H. Tang, K.E. Miller, and G. Dryhurst, Increased Extracellular Glutamate Evoked by 1-Methyl-4-Phenylpyridinium (MPP +) in the Rat Striatum is Not Essential For Dopaminergic Neurotoxicity and Is Not Derived From Released Glutathione. Neurotoxicity Res. 7:251-263, 2005-.
Schechter, R. and K.E. Miller, Insulin Effects on Neurofilament Phosphorylation. in New Research on Neurofilament Proteins, Ruby K. Arlen, ed., Chapter 6, Nova Publishers, 2006.
Ghosh, C., M. Storey-Workley, S. Usip, J. Hafemeister, K.E. Miller, and R.E. Papka, Glutamate and metabotropic glutamate receptors associated with innervation of the uterine cervix during pregnancy: receptor antagonism inhibits c-Fos expression in rat lumbosacral spinal cord at parturition. J. Neurosci. Res. 85(6):1318-35. 2007.
E.M. Hoffman, R. Schechter, K.E. Miller, Fixative composition alters distributions of immunoreactivity for glutaminase and two markers of nociceptive neurons, Nav1.8 and TRPV1, in the rat dorsal root ganglion. J. Histochem. Cytochem. 58(4):329-44, 2010.
E.M. Hoffman, R. Schechter, K.E. Miller, Peripheral inhibition of glutaminase reduces carrageenan-induced Fos expression in the superficial dorsal horn of the rat. Neuroscience Lett. 472(3):157-160, 2010.
Schechter, R. and K.E. Miller, Effects of Insulin on Tau and Neurofilament. in Handbook of Neurochemistry and Molecular Neurobiology, Editor-in-chief: Lajtha, Abel, Springer, 2010.
Miller K.E., E.M. Hoffman,and R. Schechter, Glutamate pharmacology and metabolism in peripheral primary afferents: physiological and pathophysiological mechanisms. Pharmacology & Therapeutics (invited review), 2010.
Miller K.E., K.E. Edwards, J. Balbás, A.B. Richards, R. Benton, R. Schechter, and R.M. Kriebel, Glutaminase immunoreactivity and enzyme activity is increased in the rat dorsal root ganglion following inflammation. (in revision) 2010.
E.M. Hoffman, K.M. Edwards, K.E. Miller, Glutaminase immunoreactivity changes in rat dorsal root ganglion during unilateral adjuvant-induced arthritis. (in revision) 2010.
E.M. Hoffman, Z. Zhang, M.B. Anderson, K.M. Edwards, R. Schechter, and K.E. Miller, Nav1.8 and glutaminase expression changes in dorsal root ganglion neuron subpopulations as a potential mechanism of hypoalgesia during autoimmune nerve growth factor deprivation in the adult rat. (in revision) 2010.
Title: The focus of my research effort has been to evaluate glutamate metabolism in spinal systems during various injury, inflammatory, and pain conditions. Glutamate is the major excitatory neurotransmitter in the nervous system, but the production and degradation of glutamate is poorly understood in the peripheral nervous system. My research has been carried out in three areas: 1. Primary sensory neurons under normal and painful, inflammatory and neuropathic conditions. 2. Spinal processing of inflammatory nociceptive information from the viscera and somatic structures. 3. Response of neurons to spinal injury and CNS inflammation.
Pain is a debilitating complication of chronic inflammation and nerve injury. These chronic pains are difficult to treat for long periods of time. Our current research efforts have been directed toward glutamate metabolism during chronic inflammatory pain. We have demonstrated that the glutamate-glutamine cycle, a CNS enzyme system for the production and degradation of glutamate, is present in the peripheral nervous system. We have shown that chronic inflammation causes long-term increases in glutaminase, the enzyme for glutamate synthesis, and glutamate levels in primary sensory neurons and their peripheral nerve fibers. Increased glutamate production in peripheral nerve fibers is responsible, in part, for painful responses observed in chronic inflammations, such as rheumatoid arthritis. We have determined that peripheral inhibition of glutaminase provides long-lasting pain relief in animals with chronic inflammation.
National Institutes of Health; Role: PI; Title: Glutamate in peripheral afferents after inflammation. Dates of support: 04/01/03– 03/31/10
Oklahoma State University Center for Health Sciences; Role: PI; Title: Regulation of glutaminase for wound healing. Dates of support: 07/01/10– 06/30/11
Technology transfer from our laboratory has yielded three US patents.
Miller, K.E., Method of alleviating chronic pain via peripheral glutaminase regulation, US Patent #7,288,246, 2007.
Miller, K.E., Method of alleviating chronic pain via peripheral neurotransmitter synthesis, US Patent #7,504,231, 2009.
Miller, K.E., Method of alleviating chronic pain via peripheral glutaminase regulation, US Patent # 7,714,007, 2010.