Indiana University

Fletcher A. White, Ph.D.

Professor and V.K. Stoelting Chair of Anesthesia
Professor of Pharmacology & Toxicology

Education / Training:
M.S.: Medical College of Ohio, Toledo, OH (Pathology, 1990)
Ph.D.: Medical College of Ohio Toledo, OH (Anatomy/Neurobiology, 1994)
Postdoctoral Fellowship: Washington University, St. Louis, MO (Neurology, 1994-1998)
Postdoctoral Fellowship: Massachusetts General Hospital/Harvard Medical School, Boston, MA (Anesthesia,1998-1999)

Cytokine/Chemokine signaling and the sensory neuron.

The focus of the White Lab is on the peripheral nervous system is the biology of the primary afferent neuron. Primary afferent neurons transduce and convey somatic sensation (touch, pressure, temperature, [warm or cold], pain [including itch and tickle] and proprioception) from peripheral target tissues (skin, muscle, viscera) to the spinal cord dorsal horn. The long-term goal of my research program is to understand the mechanisms, at the cellular and molecular level, by which primary afferent neurons function under both normal conditions and following peripheral nerve injury or disease. Research avenues directed at this goal have included axon guidance cues, neurotrophic factors, programmed cell death, heat shock proteins and most recently, cytokines and chemokines.

Damage to peripheral nerves following trauma or disease has a number of consequences including the emergence of neuropathic pain. Commonly, neuropathic pain sufferers experience spontaneous burning pain in and radiating from the area innervated by the damaged nerves, and an exquisite sensitivity to light touch stimuli, which are now perceived as painful. These neuropathic pains are often refractory to conventional analgesic therapy, with most patients obtaining at best only partial relief. Unfortunately, neuropathic pains are frequently also very persistent and do not resolve with time. Thus, neuropathic pain is often an extremely debilitating condition with a bleak outlook. Our research focus is on the pathophysiological and neural-immune mechanisms linking injury to the peripheral nervous system with structural and chemical alterations in the central nervous system causing neuropathic pain.

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Peer-reviewed Publications (Selected from 80 publications): 

  • White, FA, Waters, S.M., Sun, J., Ma, C., Ren, D., Ripsch, M., Steflik, J., Cortright, D.N., LaMotte, R.H., Miller, R.J.  (2005)  Excitatory MCP-1/CCR2 chemokine signaling is up-regulated by sensory neurons subjected to chronic injury. Proceedings of the National Academy of Science, USA, Sep 27; 102(39): 14092-7. 
  • White, FA, Bhangoo, S.K., Miller, R.J.  (2005)  Chemokines: Integrators of Pain and Inflammation. Nature Reviews: Drug Discovery, Oct;4(10):834-44.
  • Bhangoo SK Ren D, Miller RJ, Chan DM, Ripsch MS, Weiss C, McGinnis C, White FA. (2007). CXCR4 chemokine receptor signaling mediates pain hypersensitivity in association with antiretroviral toxic neuropathy. Brain, Behavior and Immunity, Jul;21(5):581-91.
  • Bhangoo S, Ren D, Miller RJ, Chan DM, Ripsch MS, White FA. (2007) Delayed expression of chemokine receptors following focal nerve demyelination is associated with the maintenance phase of a neuropathic pain state.  Molecular Pain, Dec 12;3(1):38.
  • White FA, Jung H, Miller RJ. (2007) Chemokines and the pathophysiology of neuropathic pain. Proceedings of the National Academy of Science, USA, Dec 18;104(51):20151-8.
  • Jung H, Bhangoo S, Banisadr G, Freitag C, White FA, Miller RJ. (2009) Visualization of chemokine receptor activation in vivo reveals peripheral activation of CCR2 receptors in states of neuropathic pain. Journal of Neuroscience, Jun 24;29(25):8051-62.
  • Bhangoo S, Ripsch M, Buchanan DJ, Miller RJ, White FA. (2009) Increased chemokine signaling in a model of HIV1-associated peripheral neuropathy. Molecular Pain, Aug 12;5:48.
  • White FA, Feldman P, Miller RJ. (2009) Chemokine signaling and the management of neuropathic pain. Molecular Interventions, 9(4):188-195.

  • White FA and Miller RJ. (2010) Insights into the Regulation of Chemokine Receptors by Molecular Signaling Pathways: Functional Roles in Neuropathic Pain. Brain Behavior and Immunity, 24(6):859-65.
  • Wilson NM, Jung H, Ripsch MS, Miller RJ, White FA. (2010) CXCR4 Signaling Mediates Morphine-induced Tactile Hyperalgesia. Brain Behavior and Immunity Mar;25(3):565-73.
  • Brittain JM, Duarte DB, Wilson SM, Wang Y, Zhu W, Ballard C, Khanna M, Schmutzler BS, Xiong W, Brustovetsky T, Ripsch MS, Cheong BM, Due MR, Ashpole N, Hingtgen CM, Brustovetsky N, Hudmon A, Jin X, Xu XM, White FA, Khanna R (2011). Suppression of inflammatory and neuropathic pain by uncoupling CRMP-2 from the presynaptic Ca2+ channel complex. Nature Medicine Jun 5;17(7):822-9.
  • Ripsch MS, Ballard CJ, Khanna M, Hurley JH, White FA, Khanna R (2012). A peptide uncoupling CRMP-2 from the presynaptic Ca2+ channel complex demonstrates efficacy in animal models of migraine and AIDS therapy-induced neuropathy. Translational Neuroscience, Mar;3(1):1-8, 2012.
  • Due MR, Piekarz AD, Khanna M, Wang B, Ripsch, MS, Wang R, Meroueh SO, Vasko MR, White FA, Khanna R (2012). CRMP-2 Peptide Mediated Decrease of Low and High Voltage-Activated Calcium Channels, Attenuation of Nociceptor Excitability, and Anti-nociception in a Model of AIDS Therapy-Induced Painful Peripheral Neuropathy. Molecular Pain, Jul 24;8(1):54. [Epub ahead of print].
  • Due MR, Piekarz AD, Wilson NM, Feldman P, Ripsch, MS, Khanna R, White FA (2012) Neuroexcitatory effects of morphine-3-glucuronide are dependent on Toll-like receptor 4 signaling. Journal of Neuroinflammation, Aug 16;9(1):200.
  • Ju W, Li Q, Allette YM, Ripsch MS, White FA, Khanna R (2012) Suppression of pain-related behavior in two distinct rodent models of peripheral neuropathy by a homopolyarginine-conjugated CRMP2 peptide . J Neurochem. Oct 26. doi: 10.1111/jnc.12070. [Epub ahead of print]