Dr. Qing Lin

Dr. Qing Lin

  • Associate Professor of Psychology
  • Email: qilin@uta.edu
  • Phone: (817) 272-0154
  • Address: Room 434, Engineering Research Building
  • Website: Click to View
  • Description of Research
    Mechanisms of Neurogenic Inflammation Induced Pain - The National Institute of Health (NIH) funded research project. Neurogenic inflammation is the process by which inflammatory mediators released from sensory nerve terminals produce inflammation in their target tissue. This process exacerbates pain. Neurogenic inflammation contributes to many clinically relevant states, including arthritis, inflammatory bowel disease, complex regional pain syndrome (CRPS), chronic bronchitis, migraine and interstitial cystitis. One of the mechanisms by which neurogenic inflammation is induced is the effector function of primary nociceptive afferent fibers. It is hypothesized that antidromic activity in primary afferents triggers the release of inflammatory mediators from these terminals when peripheral tissue is damaged, which helps develop neurogenic inflammatory pain. An increasing number of studies demonstrate that the antidromic activity of primary afferent fibers is centrally mediated by way of dorsal root reflexes (DRRs). In order to investigate its mechanisms, we have experimentally established an acute model of neurogenic inflammation by using an intradermal capsaicin (CAP) injection. The long-term goal of the proposed studies is to elucidate how neurogenic inflammation is initiated by action of the peripheral nociceptive molecule, the transient receptor potential vanilloid-1 (TRPV1) activated by CAP, then maintained by triggering the centrally mediated antidromic activity, DRRs, to exacerbate inflammatory pain, and how the released inflammatory mediators driven by DRRs participate in the process of pain sensation. Currently, our specific goals are 1) to determine if neurogenic inflammation following CAP injection involves triggering DRRs that cause the release of calcitonin gene-related peptide and/or substance P from primary afferent nociceptors and if this process would, in turn, enhance the CAP-induced sensitization of primary afferent nociceptors, as well as analyze if this process is initiated by activation of TRPV1 receptors; 2) to examine if activation of the TRPV1 receptors in primary afferent nociceptors plays an important role in enhancing DRRs by activating GABAergic interneurons in dorsal horn circuits; 3) to determine if phosphorylation of protein kinase C (PKC) takes place in the primary afferent neurons when neurogenic inflammation is initiated and develops and if TRPV1 receptors are upregulated by the phosphorylation of PKC.
    Electrophysiology, neuropharmacology, neurochemistry, immunocytochemistry (confocal imaging analysis), Western blots, and laser Doppler blood flow meter are utilized to perform these studies. In addition, we are currently developing molecular biological techniques, such as PCR, aiming at a deeper study of ionic and molecular targets by which the DRRs mediate inflammatory pain.
    Uncovering these mechanisms will be critical for pharmaceutical manufacturers and clinicians to develop new anti-inflammatory therapies and improve the healthcare for patients. 

    Representative Publications


    1. Xu X., Wang P., Zou X., Li D., Fang L., Lin Q. Increases in transient receptor potential vanilloid-1 mRNA and protein in primary afferent neurons stimulated by protein kinase C and their possible role in neurogenic inflammation. J Neurosci Res 87:482-494, 2009.

    2. Li D, Ren Y, Xu X, Zou X, Fang L, Lin Q. Sensitization of primary afferent nociceptors induced by intradermal capsaicin involves the peripheral release of calcitonin gene-related peptide driven by dorsal root reflexes. J Pain 9:1155-1168, 2008.

    3. Lin Q, Li D, Xu X, Zou X, Fang L. Roles of TRPV 1 and neuro-peptidergic receptors in dorsal root reflex-mediated neurogenic inflammation induced by intradermal injection of capsaicin. Mol Pain 3:30, 2007.

    4. Ren Y, Zou X, Fang L, Lin Q. Involvement of peripheral purinoceptors in sympathetic modulation of capsaicin-Induced sensitization of primary afferent fibers. J Neurophysiol 96:2207-2216, 2006.

    5. Lin, Q., Cervero, F., and Schmelz, M. Pathophysiology of neurogenic inflammation. In Flor, H., Kalso, E., and Dostrovsky, J.O. (eds). Proceedings of the 11th World Congress on Pain. IASP Press, Seattle 2006, p155-168.

    6. Ren Y, Zou X, Fang L, Lin Q. Sympathetic modulation of activity in Aδ and C primary afferents following intradermal injection of capsaicin in rats. J Neurophysiol 93:365-377, 2005.

    7. Lin Q, Zou X, Ren Y, Wang J, Fang L, Willis WD. Involvement of peripheral neuropeptide Y receptors in sympathetic modulation of acute cutaneous flare induced by intradermal capsaicin. Neuroscience123:337-347, 2004.

    8. Wang J, Ren Y, Zou X, Fang L, Willis WD, Lin Q. Sympathetic influence on capsaicin-evoked enhancement of dorsal root reflexes in rats. J Neurophysiol92:2017-2026, 2004.

    9. Lin Q, Zou X, Fang L, Willis WD. Sympathetic modulation of acute cutaneous flare induced by intradermal injection of capsaicin in anesthetized rats. J Neurophysiol89:853-861, 2003.

    10. Lin, Q. A contribution of dorsal root reflexes to neurogenic inflammation and pain. In Chen, J., Chen, A.C.N., Han, J.S., and Willis, W.D. (eds), Experimental Pathological Pain: from Molecules to Brain Functions. Science Press, Beijing, 2003, p36-56.

    11. Zou X, Lin Q. Willis WD. The effects of sympathectomy on capsaicin-evoked Fos expression of spinal dorsal horn GABAergic neurons. Brain Res958:322-329, 2002.