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Neuroscience PhD at Wake Forest University at Wake Forest University

Wake Forest University Graduate School » Neuroscience PhD at Wake Forest University

Christopher Peters

Christopher Peters
Dr. Peters obtained his B.S. in Biochemistry and Molecular Biology in 1994 from the University if Miami. In 2007, he received his PhD in Microbiology, Immunology and Cancer Biology at the University of Minnesota where he studied the cellular mechanisms that contribute to cancer related pain in rodent models of bone cancer pain and chemotherapy induced neuropathy.


Chronic pain after surgery (CPAS) is now recognized as a major public health concern which can affect between 10 and 50% of patients depending on the type of surgery. Currently, there is no standard of medical care provided perioperatively to prevent CPAS. This is due in part to an incomplete knowledge of the risk factors and biological mechanisms that are responsible for postoperative pain transitioning from an acute stage that resolves with wound healing to a more chronic pain state. Various surgical, biological, inter-individual, and psychosocial factors are associated with a greater incidence of CPAS. Recent clinical studies report that patients with diminished preoperative endogenous pain inhibition are at greater risk for developing CPAS. We modeled this observation in rodents by disrupted spinally projecting noradrenergic neurons prior to surgery using a targeted toxin (dopamine β hydroxylase conjugated to saporin). This manipulation results in prolonged mechanical hypersensitivity (Figure 1) and increased spinal glial activation in rats after plantar incision (Brennan incision model). Project1-Peters Figure 1: Disruption of spinal noradrenergic fibers prior to surgery using a targeted toxin (DβH-saporin) increased the duration of mechanical hypersensitivity following plantar incision in the rat. Longitudinal behavioral data is expresses as group averaged values (line and symbol) and modeled for treatment groups and individual rats using growth curve analysis (dashed lines with 95% CI) to examine changes over time of postoperative pain trajectory.
Under NIH grant GM99863, we are studying how disrupting spinal noradrenergic signaling influences spinal neural and glial plasticity (Figure 2) promoting the transition from acute to a more persistent postoperative pain state. We use a combination of in vivo biochemical, pharmacological, behavioral and immunohistochemical methods as well as in vitro primary microglial and astrocyte cultures as part of these studies. Research in the Pain Mechanisms lab is also focused on monitoring postoperative pain related behaviors over time using mixed effects growth curve modeling. This type of analysis gives rise to intercept (initial pain at time 0), slope (linear rate of change in pain measure), and quadratic term (acceleration and deceleration over time reflecting inflections in change during recovery) parameters. The intercept, slope and quadratic term estimates can vary across individual rats (random effects) and as a function of treatment group or condition (fixed effects) allowing us to examine the ability of socio-environmental conditions or pharmacological interventions to impair or improve several aspects of postoperative pain trajectory. The ultimate goal of this research is to identify FDA approved and novel therapeutic approaches for preventing CPAS to introduce into clinical studies. Peters proj2-500 Figure 2: Potential mechanisms by which reduced spinal noradrenergic signaling contributes to the transition from acute to chronic postoperative pain.


  1. Yaksh TL, Hobo S, Peters C, Osborn KG, Richter PJ Jr, Rossi SS, Grafe MR, Eisenach JC. Preclinical toxicity screening of intrathecal oxytocin in rats and dogs. Anesthesiology. 2014;120(4):951-961.
  2. Peters CM, Ririe D, Houle TT, Aschenbrenner CA, Eisenach JC. Nociceptor-selective peripheral nerve block induces delayed mechanical hypersensitivity and neurotoxicity in rats. Anesthesiology. 2014;120(4):976-986.
  3. Lombardo S, Peters C, Eisenach J. The effects of nerve injury on the expression of vasopressin receptor V1aR in the dorsal root ganglia [abstract]. J Pain. 2014;15(4 Suppl 1):S48.
  4. Hayashida K-i, Peters CM, Gutierrez S, Eisenach JC. Depletion of endogenous noradrenaline does not prevent spinal cord plasticity following peripheral nerve injury. J Pain. 2012;13(1):49-57.
  5. Peters CM, Eisenach JC. Contribution of the chemokine (C-C motif) ligand 2 (CCL2) to mechanical hypersensitivity after surgical incision in rats. Anesthesiology. 2010;112(5):1250-1258.
  6. Peters CM, Hayashida K-i, Ewan EE, Nakajima K, Obata H, Xu Q, Yaksh TL, Eisenach JC. Lack of analgesic efficacy of spinal ondansetron on thermal and mechanical hypersensitivity following spinal nerve ligation in the rat. Brain Res. 2010;1352():83-93.