Fletcher A. White, Ph.D.

 

Professor and V.K. Stoelting Vice Chair of Anesthesia

Professor of Pharmacology & Toxicology

 

Education / Training:

BA, Psychology, Baldwin-Wallace College, Berea, OH (1985)

MS, Pathology, Medical College of Ohio, Toledo, OH (1989)

PhD, Neurobiology, Medical College of Ohio, Toledo, OH (1994)

Postdoctoral, Washington University, St. Louis, MO (1994-1998)

Postdoctoral, Harvard Medical School, Boston, MA (1998-1999)

Cytokine/Chemokine signaling and the sensory neuron.

The focus of the White Lab is the peripheral nervous system and 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.

Recent Publications

  • ZhangHJ, Mei XF, Ma C,Donnelly DF, White FA, LaMotte RH.  Altered functional properties of satellite glial cells following a chronic compression of the rat dorsal root ganglion.
    Glia, Mar 29 [epublished online], 2009.
  • Jung H, Bhangoo S, Banisadr G, Freitag C, White FA, Miller RJ. 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, 2009
  • Bhangoo S, Ripsch M, Buchanan DJ, Miller RJ, White FA.  Increased chemokine signaling in a model of HIV1-associated peripheral neuropathy.Molecular Pain, 5:48, 2009.
  • Wilson NM, Jung H, Ripsch MS, Miller RJ, White FA. CXCR4 Signaling Mediates Opioid-induced Hyperalgesia.Brain Behavior and Immunity, Mar;25(3):565-73, 2011.
  • 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. Suppression of inflammatory andneuropathic pain by uncouplingCRMP-2 from the presynaptic Ca2+ channel complex.
    Nature MedicineJun 5;17(7):822-9,2011
  • Moser RM, Jung J,Farooq A, McClung C, Fitzgerald MP, White FA.Sciatic nerve injury induces expression of functional pro-nociceptive chemokine receptors in bladder-associated primary afferent neurons in the rat. NeuroscienceJun 2;183:230-7, 2011
  • Kohn H, Wang Y, Wilson SM, Brittain JM, Ripsch MS, Salome C, Park KD Park, White FA, Khanna R. Merging Structural Motifs of Functionalized Amino Acids and α-Aminoamides Results in Novel Anticonvulsant Compounds with Significant Effects on Slow and Fast Inactivation of Voltage-gated Sodium Channels and in the Treatment of Neuropathic Pain.ACS Chemical Neuroscience Jun 15;2(6):317-322, 2011
  • Brittain JM, Chen L, Brustovetsky T,  Gao X, Ashpole N, Wilson SM, Hudmon A, Brustovetsky N, Chen J, White  FA, Khanna R Neuroprotection against traumatic brain injury by a peptide derived from the collapsin response mediator protein 2 (CRMP-2).
    Journal of Biological Chemistry, Oct 28;286(43):37778-92, 2011
  • Wilson SM, Brittain JM, Piekarz, AD, Ballard CJ, Ripsch MS, Cummins TR, Hurley JH, Khanna M, White FA, Khanna R. Further insights into the antinociceptive potential of uncoupling calciumchannels (CaV2) from the collapsin response mediator protein-2 (CRMP-2).Channels (Austin) Sep 1;5(5):449-56, 2011
  • Ripsch MS, Ballard CJ, Khanna M, Hurley JH, White FA, Khanna R.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.
  • Wilson SM, Ripsch MS, White FA, Khanna R.Inhibition of Transmitter Release and Attenuation of AIDS Therapy-Induced Painful Peripheral Neuropathy by Synthetic Ca2+ Channel Peptides.Journal of Biological Chemistry, accepted.
  • Feldman P, Due MR, Ripsch MS, Khanna R,  White FA.The persistent release of HMGB1 contributes to tactile hyperalgesia in a rodent model of neuropathic pain. Journal of Neuroinflammation, accepted.

 

Book Chapters

  • Sommer C, White FA.Cytokines, Chemokines, and Pain. In: Beaulieu P, Lussier D, Porreca F, Dickenson AH (eds.),  Pharmacology of Pain.International Association for the Study of Pain Press, 2010.
  • Bhangoo S, Petty L, White FA Animal Models of HIV-associated Painful Sensory Neuropathy, In: Zhang J, Ma C (eds.), Neuromethods: Animal Models of Pain. Springer Humana Press, 2011.