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
     

    NEUROBIOLOGY OF PAIN, NEUROTOXIC IMPACT ON THE DEVELOPING BRAIN, AND DEMYELINATING OPTIC NEURITIS

    1. Pain and pain medicine study: We are currently focusing on developing a new animal model of chronic migraine headache. Specifically, we are interested in exploring a way of how the chronification develops contributing to the acute-to-chronic transition of migraine headache induced by aversive (affective) environments, which would significantly mimic the cases mostly seen in the migraine patients. We will then investigate the underlying neural mechanisms.
    2. Neurotoxicity of anesthetics in the developing brain: The research has focused on examining whether the vulnerability to the neurotoxic effects of the anesthetic, ketamine, in immature brain neurons is due to molecular and pharmacological properties of NMDA-type glutamate receptors distinct from that in mature brain neurons. The project establishes a pathological link between the higher sensitivity of NMDA receptor response to ketamine exposure and the development of neuroapoptosis in the developing brain.
    3. Remyelinating mechanism in relapsing-remission neuromyelitis optica (NMO): Invited to participate in an international collaborative project entitled “A Study on the Development of New Research Approaches Used in the Evaluation and Diagnosis of the Neurodegenerative Disorders of Optical Neuritis” Specifically, we have studied molecular mechanisms underlying demyelinating and remyelinating processes occurring in the pathogenesis of NMO by using an animal model of demylenation. The CXC chemokines (CXC-motif ligand 12 and CXC-motif ligand 14) are suggested to play a modulatory role in remyelination in the course of many demyelinated diseases. Our data indicate that the prognosis of neuritis depends on remyelinating process that is impaired due to decreased chemokines. The much lower levels of chemokines would specifically indicate the severe neuritis, such as NMO.
     

    Representative Publications

    1. Gong K, Zou X, Fuchs NP, Lin Q. Minocycline inhibits neurogenic inflammation by blocking the effects of tumor necrosis factor-α. Clin Exp Pharmacol Physiol 42:940-949, 2015. Corresponding Author.

    2. Sun W, Yang F, Wang Y, Fu H, Yang Y, Li C-L, Wang X-L, Lin Q, Chen J. Contribution of large-sized primary sensory neuronal sensitization to mechanical allodynia by upregulation of hyperpolarization-activated cyclic nucleotide gated channels via cyclooxygenase 1 cascade. Neuropharmacology 113:217-230, 2017. Corresponding Author.

    3. Wang R, Wang Y, Guan S-M, Li Z; Kokane S, Cao F-L, Sun W, Li C-L, He T, Yang Y, Lin Q, Chen J. Synaptic homeostasis and allostasis in the dentate gyrus caused by  inflammatory and neuropathic pain conditions. Front Synaptic Neurosci. PMID: 29445338 PMCID: PMC5797731 DOI: 10.3389/fnsyn.2018.00001, 2018. Corresponding Author.

    4. Jin J, Gong K, Zou X, Lin Q, Chen J. The blockade of NMDA receptor ion channels by ketamine is enhanced in developing rat cortical neurons. Neurosci Lett 539:11-15, 2013. Corresponding Author.

    5. Wang R, Jin J, Womack AW, Lyu D, Kokane SS, Tang N, Zou X, Lin Q, Chen J. Neonatal ketamine exposure causes impairment of long-term synaptic plasticity in the anterior cingulated cortex of rats. Neuroscience 268:309-317, 2014. Corresponding Author.

    6. Stevens RA, Butler BD, Kokane S, Womack A, Lin Q. Neonatal inhibition of Na+-K+-2Cl- cotransporter prevents ketamine induced spatial learning and memory impairments. Neurotoxic Teratol 60:82-86, 2017. Corresponding Author.

    7. Kokane SS, Gong K, Jin J, Lin Q. Prolonged ketamine exposure induces increased activity of the GluN2Bcontaining N-methyl-D-aspartate receptor in the anterior cingulate cortex of neonatal rats. Neurotoxic Teratol 63:1-8, 2017. Corresponding Author.

    8. Kokane SS, Lin Q. Impact of early life ketamine exposure on the developing brain and cognitive sequelae: A discussion of apoptotic neurodegeneration mechanisms, In Preedy VR (ed). The Neuropathology of Drug Addictions and Substance Misuse (Chapter 54). Kings College London, 2016, p581-592. Corresponding Author.

    9. Chen T, Li Z, Jiang Z, Liu Z, Xu Q, Huang D, Lin Q, Wei S. Changes of CXCL12, CXCL14 and PDGF levels in the brain of patients with idiopathic demyelinating optic neuritis and neuromyelitis optica. J Neuroimm 279:1-6, 2015. Corresponding Author.

    10. Kang H, Cao S, Chen T, Jiang Z, Liu Z, Li Z, Xu Q, Lin Q,  Wei S. The poor recovery of neuromyelitis optica spectrum disorder is associated with a lower level of CXCL12 in the human brain. J Neuroimm  289:56-61, 2015. Corresponding Author.