Education & Training
- Postdoctoral Fellow
- M.D. Anderson Cancer Center, University of Texas, Houston, 2006
- Postdoctoral Fellow
- University of Arkansas for Medicine Sciences, 2002
Areas of Interests
- Research Interest
- Chronic pain induced by spinal cord injury: mechanisms and potential treatments
My long-term research interest is to understand mechanisms underlying chemotherapy and traumatic injury-induced neuropathy with a major goal to identify potential therapeutic targets that can be used to effectively treat chemotherapy- and traumatic injury-induced complications. At present, I seek to deconstruct the role of ion channels in spinal cord injury (SCI)-induced secondary degeneration and chemotherapy-induced peripheral neuropathy (CIPN) to gain new insight on the treatment.
- One research in lab focus on the identifying molecular mechanism underlying CIPN, as well as a potential therapeutic target to prevent the development of CIPN, including chronic pain. Excessive neuronal excitation is a primary source of CIPN. My goal is to identify the channelopathy that involved in CIPN-induced over-excitation of primary sensory neurons, and try to identify novel targets for therapeutic development.
- Another research focus on the contribution of ion channels in neuroprotection and axon regeneration after spinal cord injury (SCI). Traumatic injury to the spinal cord results in acute necrosis and secondary degeneration of spinal tissues, followed by a chronic stage with cavities and scar tissue formed, leaving the individual living with paralysis, and sensory dysfunction. Mild or strong neuronal excitations are at the core of injury evoked by various insults, necrotic neuronal damage often is a fee paid for excessive excitation. Thus, decreasing neuronal excitability by modulating some ion channels would be a useful strategy to treat SCI-induced complications in both acute and chronic phases.
- Yin S*, Luo J*, Qian A, Du J, Yang Q, Zhou S, Yu W, Du G, Clark RB, Walters ET, Carlton SM, Hu H. (2013). Retinoids activate the irritant receptor TRPV1 and produce sensory hypersensitivity. J Clin Invest 123(9):3941-51.
- Bedi SS*, Yang Q*, Crook RJ*, Du J, Wu ZZ, Fishman H, Grill RJ, Carlton SM, Walters ET. Chronic spontaneous activity generated in the somata of primary nociceptors is associated with pain-related behavior after spinal cord injury. (* equal contribution) J Neurosci 30(44):14870-14882.
- Li DP, Yang Q, Pan HM, Pan HL. (2008) Plasticity of pre- and postsynaptic GABAB receptor function in the paraventricular nucleus in spontaneously hypertensive rats. Am J Physiol Heart Circ Physiol 295(2): H 807-815.
- Li DP, Yang Q, Pan HM, Pan HL. (2008) Pre- and postsynaptic plasticity underlying augmented glutamatergic inputs to hypothalamic presympathetic neurons in spontaneously hypertensive rats. J Physiol 586(6): 1637-1647.
- Li DP, Yang Q. (2007) Membrane and synaptic properties of nucleus tractus solitarius neurons projecting to the caudal ventrolateral medulla. Auton Neuroscience 136(1-2):69-81.
- Yang Q, Chen SR, Li DP, Pan HL. (2007) Kv1.1/1.2 Channels are downstream effectors of nitric oxide on synaptic GABA release to pre-autonomic neurons in the paraventricular nucleus. Neuroscience 149 (2):315-327.
- Yang Q, Sumner AD, Puhl HL, Ruiz-Velasco V. (2006) M (1) and M (2) muscarinic acetylcholine receptor subtypes mediate Ca2+ channel current inhibition in rat sympathetic stellate ganglion neurons. J Neurophysiol 96(5): 2479-2487.