Personal Profile

Professor Liu Xianguo was born in February 1957 in Naiman Banner, Inner Mongolia. He is currently a professor and director of the Physiology Teaching and Research Section in the School of Basic Medical Sciences, a doctoral supervisor, the director of the Pain Research Center at Sun Yat-sen University, and the vice dean of the Zhongshan School of Medicine, Sun Yat-sen University.

Educational Background

• October 1992 - April 1995: Second Institute of Physiology, Heidelberg University, Germany. Obtained a Doctor of Philosophy degree.
• September 1985 - August 1988: Physiology Teaching and Research Section, Bethune Medical University. Obtained a Master of Science degree.
• March 1978 - December 1982: Medical Department, Yanbian Medical College. Obtained a Bachelor of Science degree.

Work Experience

• June 1999 - Present: Director of the Physiology Teaching and Research Section, Professor at Sun Yat-sen University.
• May 1997 - May 1999: Postdoctoral Fellow at the Institute of Physiology, Kiel University, Germany.
• May 1995 - April 1997: Postdoctoral Fellow at the Second Institute of Physiology, Heidelberg University, Germany.
• September 1988 - September 1992: Lecturer in the Physiology Teaching and Research Section, North China Coal Medical College.
• January 1983 - August 1985: Assistant in the Physiology Teaching and Research Section, Inner Mongolia National Medical College.

Academic Achievements
Published Papers

1. BDNF induces late-phase LTP of C-fiber evoked field potentials in rat spinal dorsal horn

2. Peri-sciatic administration of recombinant rat TNF-α induces mechanical allodynia via up-regulation of TNF-α in dorsal root ganglia and in spinal dorsal horn: the role of NF-kappa B pathway. Experimental Neurology, 205:471-484。

3. p38 activation in uninjured primary afferent neurons and in spinal microglia contributes to the development of neuropathic pain induced by selective motor fiber injury. Experimental Neurology, 204 (1): 355-365.

4. Tumor necrosis factor-alpha induces long-term potentiation of C-fiber evoked field potentials in spinal dorsal horn in rats with nerve injury: The role of NF-kappa B, JNK and p38 MAPK. Neurophamarcology, 52：708-715.

5. NMDA receptor channels are involved in the expression of long-term potentiation of C-fiber evoked field potentials in rat spinal dorsal horn. Progress in biochemistry and biophysics, 33 (12): 1183-1189.

6. Clonidine depresses LTP of C-fiber evoked field potentials in spinal dorsal horn via NO-cGMP pathway. Brain Res, 1118 (1): 58-65.

7. Inhibition of protein tyrosine kinases attenuated Aβ-fiber-evoked synaptic transmission in spinal dorsal horn of rats with sciatic nerve transection. J Pharmacol Sci, 102 (1): 64-71.

8. The role of phosphorylation of ERK in induction and maintenance of LTP of the C-fiber evoked field potentials in spinal dorsal horn. J Neurosci Res, 84(5): 934-43.

9. The role of tumour necrosis factor-alpha in the neuropathic pain produced by lumbar 5 ventral root transection in rat. Pain, 123:306-321.

10. Diazepam inhibits the induction and maintenance of LTP of C-fiber evoked field potentials in spinal dorsal horn of rats. Neuropharmacology, 50(2): 238-244.

11. Activation of Spinal D1/D5 Receptors Induces Late Phase LTP of C-fiber Evoked Field Potentials in Rat Spinal Dorsal Horn. J Neurophysiol, 94 (2):961-967.

12. PKC在成年大鼠脊髓背角C－纤维诱发电位长时程增强的诱导和维持中的作用。中国病理生理学杂志，21（2）；252－255。

13. Acute nerve injury induces LTP of C-fiber evoked field potentials in spinal dorsal horn of intact rat. Sheng Li Xue Bao，56:591-596.

14. KN-93抑制脊髓背角C 纤维诱发场电位长时程增强的诱导和早期表达。中山大学学报，24（4）：109-113。

15. 刺激Aδ纤维可抑制背角C-纤维诱发电位长时程增强.中国临床康复，7（10）：1510-1512。(

16. 磷酸化CaMKII 在脊髓背角C-纤维诱发LTP诱导和维持中的作用。生理学报， 56 (1)： 83-89。

17. 髓背角II板层在长时程增强诱导及维持过程中的突触形态计量学研究。生理学报，56:397-402。

18. The roles of CAMKII, PKA and PKC in the induction and maintenance of LTP of c-fiber evoked field potentials in rat spinal dorsal horn. J Neurophysiol，91 (3):1122-1133.

19. Induction of long-term potentiation of C fibre-evoked spinal field potentials requires recruitment of group I, but not group II/III metabotropic glutamate receptors. Pain 106: 373-379.

20. Protein synthesis inhibition blocks the late-phase LTP of C-fiber evoked field potentials in rat spinal dorsal horn. J. Neurophysiol. 89: 2354-2359.

21. Time-dependent plasticity produced long-term potentiation of C-fiber evoked field potentials in rat spinal dorsal horn. Neurosci. Lett., 315: 81-84

22. Sympathetic-sensory coupling after L5 spinal nerve lesion in the rat and its relation to changes in dorsal root ganglion blood flow. Pain, 87: 335-45

23. Spontaneous activity of axotomized neurons after L5 spinal nerve injury in rats. Pain, 84:309-318.

24. Axotomized and intact muscle afferents but no skin afferents develop ongoing discharges of dorsal root ganglion origin after peripheral nerve lesion. J. Neurosci, 20:2742-2748.

Important Academic Research Achievements and Contributions

He has long been engaged in the research of the central and peripheral mechanisms of pathological pain. He has published more than twenty research papers in SCI-indexed journals, which have been cited nearly 500 times. His main academic achievements include:

1. He first reported the long-term potentiation (LTP) of C-fiber-evoked potentials in the dorsal horn of the spinal cord. He found that the activation of NMDA, NK1, and NK2 receptors is a necessary condition for inducing LTP; natural pain stimuli can cause LTP of C-fiber-evoked potentials, but it is inhibited by the descending inhibitory system under normal circumstances. This LTP is considered the basis of hyperalgesia. He also discovered that the early maintenance of spinal LTP is related to the activation of PKA, PKC, and CaMKII, while the late maintenance of spinal LTP requires new protein synthesis. Dopamine D1/D5 receptors play an important role in the late maintenance of LTP.
2. He found that electrical stimulation of Aδ fibers causes LTD of C-fiber-evoked potentials in normal animals, while the same stimulation causes LTP in spinalized animals, confirming that the descending inhibitory system determines the direction of synaptic plasticity changes in the dorsal horn of the spinal cord.
3. He was the first to confirm that the abnormal discharge of dorsal root ganglion neurons caused by nerve injury mainly comes from neurons innervating muscles. In the case of nerve injury, uninjured neurons also produce abnormal discharges.
4. He discovered that injury to the motor nerve (L5 ventral root) causes upregulation of TNF-α and its receptor 1 (TNFR1) in the ipsilateral dorsal root ganglion and bilateral dorsal horns of the spinal cord, and confirmed that TNF-α is involved in the formation but not the maintenance of pathological pain. In normal animals, different concentrations (10 pg/ml, 4.5 ng/ml, and 100 ng/ml) of TNF-α do not affect the LTP of C-fiber-evoked potentials in the dorsal horn of the spinal cord induced by tetanic stimulation. However, in animals with hyperalgesia caused by injury to the L5 ventral root, a low dose of TNF-α (10 pg/ml) can cause LTP of C-fiber-evoked potentials in the dorsal horn of the spinal cord. TNF-α exerts its effects by activating NF-κB, JNK, and P38.

Academic Affiliations

Chairman of the Guangdong Society of Physiology
Standing Committee Member of the Pain Medicine Branch of the Guangdong Medical Association
Executive Director of the Chinese Physiological Society
Member of the American Society for Neuroscience