Education
1987
Postdoctoral (Cell Biology & Neuroanatomy)
University of Minnesota
Minneapolis, MN
1984
Ph.D. (Anatomy & Neruobiology)
University of Vermont
Burlington, Vermont
1978
B.S. (Biology)
Kansas State University
Manhattan, KS
Professional Experience
2002-present
Associate Professor Department Anatomy & Cell Biology, Oklahoma State University Center for Health Sciences (OSU-CHS), Tulsa, OK
1998-2002
Assistant Professor Department Cell Biology, University of Oklahoma College of Medicine (OU COM), Oklahoma City, OK
1990-1998
Assistant Professor Department of Anatomical Sciences,OU COM
1990
Group Leader Analgesia Program, G.D. Searle & Co. Research & Development, Skokie, IL
1988-1990
Research Scientist Neurotrophic Factors Program, G.D. Searle R&D, Monsanto CO and Chesterfield, MO
1987-1988
Research Assistant Professor Department Neurol Surgery Miami Project to Cure Paralysis, Univeristy of Miami, Miami, FL
1984-1987
Postdoctoral Fellow Department of Cell Biology and Neuroanatomy, University of Minnesota, Minneapolis, MN
Other Experience
2003-2005, 1991-1993
Executive Committee, Oklahoma Center for Neuroscience
1998
Experimental Biol. Meeting Symposium organizer - “Glutamine and Glutamate Metabolism: Organ Specific Regulation”
1995-1998
Education Committee, Society for Neuroscience
1991-1993
President, Oklahoma Chapter, Society for Neuroscience
Publications
Papka, R.E., B. Srinivasan, K.E. Miller, and S. Hayashi, Localization of estrogen receptor protein and estrogen receptor mRNA in peripheral autonomic and sensory neurons. Neuroscience 79:1153-1163, 1997.
Zhang, J., M.J. Chandler, K.E. Miller, and R.D. Foreman, Cardiopulmonary sympathetic afferent input does not require dorsal column pathways to excite C1-C3 spinal cells in rats. Brain Res. 771:25-30, 1997.
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 .
Miller, K.E., J. Bálbas, B.A. Richards, R. Benton, R.M. Kriebel, Glutaminase immunoreactivity and enzyme activity is increased in the rat dorsal root ganglion following inflammation. (in revision), 2006.
Benton, R.L., C.D. Ross, J.M. Jacob, and K.E. Miller, Temporal and spatial analysis of GFAP levels in spinal white and gray matter following methylprednisolone treatment of spinal cord injury. (in revision), 2006.
Benton, R.L., C.D. Ross, and K.E. Miller, The effect of methylprednisolone treatment on glutamate levels and glial glutamate metabolism in the injured spinal cord. (in revision), 2006.
Miller, K.E., C.D. Ross, R.L. Benton, R.M. Kriebel., and R.D. Foreman, Peripheral pattern of glutamate and glutaminase immunoreactivity in rat skin: Increased immunoreactivity following chronic inflammation. (submitted), 2006.
Research
Ongoing
Title:
Glutamate in primary afferents following inflammation. Funding sources: NIH (AR047410; PI: Kenneth E. Miller); Pain is a debilitating complication during chronic inflammation and difficult to treat for long periods of time. During inflammation, the release of glutamate in skin and joints causes sensitization of sensory neurons, augmenting noxious signals sent to the spinal cord. 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. Studies are in progress to determine what cellular mechanisms cause sensory neurons to increase glutamate metabolism. Three recent papers have been published or submitted from this project (Miller et al., 2002, 2006a-b).
Agency: National Institutes of Health; Role: PI; 40% commitment; Title: Glutamate in peripheral afferents after inflammation. Dates of support: 04/01/03– 03/31/07; Direct Costs: $900,000
Title: C1-2 Modulation of Spinal Processes: Supraspinal Effects . Funding sources: NIH (NS 035471; PI: Robert D. Foreman); The long term objective is to understand the organization and role of C1-C2 neurons in the spinal cord. Our current interests lies in examining the influence that supraspinal nuclei (parabrachial/ subcoeruleus, amygdala) have in modulating C1-C2 neuronal activity. Five recent papers have been published or submitted (Miller et al., 1998; Qin et al., 1999, 2001, 2003a-b) from this project.
Agency: National Institutes of Health; Role: Project Co-I; 25% effort; Title: C1-2 Modulation of Spinal Processes: Supraspinal Effects; Dates of support: 07/01/02 - 06/30/07; Total Award: $1,455,000; (PI: Robert Foreman, Dept. Physiology, Univ. Oklahoma Health Sciences Center [OUHSC])
Title: Spinal Hierarchy and Noxious Cardiac Sensory Processing . Funding sources: NIH (HL 075524; PI: Robert D. Foreman); The purpose of this project is to evaluate how cardiac-related vagal and sympathetic sensory inputs influence upper cervical (C1-C2) and upper thoracic (T3-T4) spinal neurons to ultimately modify efferent neuronal output to the heart. We hypothesize that, within the hierarchy of neural control that regulates cardiac function, neurons in C1-C2 spinal cord influence the processing of cardiac sensory information in upper thoracic neurons, and thereby determine autonomic outflow to the heart.
Agency: National Institutes of Health; Role: Project Co-I; 25% effort; Title: Spinal Hierarchy and Noxious Cardiac Sensory Processing ; Dates of support: 05/15/04 - 04/30/08; Total Award: $1,398,505; (PI: Robert Foreman, Dept. Physiology, OUHSC)
Completed
Title: Glutamate/glutamine metabolism following spinal cord injury. Funding sources: OUHSC Dept Cell Biology and Oklahoma Center for Neuroscience Collaborative Research Grant; Our aim has been to determine h ow spinal injury affects the long-term regulation of glutamate metabolism in the spinal cord. We have found that both spinal injury and methylprednisolone, its current therapy, have dramatic effects on glutamate metabolism in neurons and glia, often in a detrimental fashion. Current studies are directed to decrease glial scarring for the promotion of nerve fiber regrowth. Two papers have been published from this research (Benton et al., 2000, 2001) and two have been submitted and are in revision (Benton et al., 2005a,b).
Agency: Oklahoma Center for Neuroscience Collaborative Research Grant; Role: Co-PI; 25% effort; Title: Effects of methylprednisolone on the development of autonomic dysreflexia; Dates of support: 07/01/01/-6/30/02. TOTAL AWARD: $19,851.
Patents
Technology transfer from our laboratory has been pursued via two patent applications over the past three years.
Miller, K.E., Method of Alleviating Chronic Pain via Peripheral Glutaminase Regulation, US Patent Application 10/245,098 (Pub. #20030072746). Sept. 13, 2002.
Miller, K.E., Method of Alleviating Chronic Pain via Peripheral Neurotransmitter Synthesis, US Patent Application. (Pub #20040126368). Sept. 13, 2003.
