Xu, Zao C., MD, PhD


  • Guangzhou Medical College, China, MD, 1982
  • Sun Yet-Sen University of Medical Sciences, China, MS, 1986
  • University of Tennessee, Memphis, PhD, 1990
  • University of Tennessee, Memphis, Postdoctoral Fellowship, 1990-1992


Academic Appointments

  • 2008 – Present Director, Confucius Institute in Indianapolis, IUPUI.
  • 2004 – Present Professor, Indiana University School of Medicine. Department of Anatomy and Cell Biology, Department of Neurology.
  • 1998 - 2004 Associate Professor, Indiana University School of Medicine. Department of Anatomy and Cell Biology, Department of Neurology.
  • 1992 - 1997 Assistant Professor, University of Tennessee, Memphis. Department of Neurology.
  • 1990 – 1992 Postdoctoral Fellow, University of Tennessee, Memphis,
  • 1982 - 1984 Instructor, Guangzhou Medical College, Department of Anatomy, Guangzhou, China.


CV in PDF format

Excitotoxicity is the major cause of neuronal damage in many neurological disorders such as stroke and traumatic brain injury. Imbalance of excitation and inhibition also results in epilepsy. The excitablity of the brain is determined by synaptic transmission and neuronal membrane property. Recent study also indicates that inflammation also plays an important role in neuronal injury in many neurological disorders.  The research in my lab is to reveal the role of alteration of neuronal excitability in pathogenesis of neurological disorders. The current projects are active in my lab:

  1. Stroke is the leading cause of death and disability in U.S. Transient cerebral ischemia results in selective neuronal damage in the brain. A-type potassium current (IA) plays important role in maintaining neuronal excitability. We have demonstrated that enhancement of IA protects neurons against ischemia. We are investigating the PKC regulation of IA channels after ischemia using animal models of transient global ischemia and oxygen-glucose deprivation models of neuronal culture.  Diabetes exacerbates the ischemia outcome and increases the incidence of post-ischemia seizure/epilepsy.  We also reveal the mechanisms of epilepsy after ischemia in normoglycemic and diabetes conditions.
  2. Seizure/epilepsy is a common sequela of acute neurological disorders including stroke and traumatic brain injury. In addition to studying the excitability change after cerebral ischemia and TBI that might contribute to post traumatic epilepsy (PTE), we also investigate the possible role of inflammation factors in PTE using animal models and patient data.

We use 4-Vessel Occlusion (4-VO) model to induce transient cerebral ischemia, and Control Cortical Impact (CCI) model to induce TBI.  The techniques in my lab including, but not limited:

  1. In vivo and in vitro electrophysiological recording, such as intracellular recording the staining, patch-clamp recording on brain slices, cell culture and acute dissociated neurons,
  2. Protein, DNA and RNA analysis, gene transfection in vivo and in vitro.
  3. Morphological techniques such as histological staining, immunocytochemical staining etc.
  • Deng, P., Zhang, Y and Xu, Z. C. (2008) Inhibition of Ih in striatal cholinergic interneurons early after transient forebrain ischemia. J Cerebr Blood F Met. 28: 939-947.
  • Zhang, Y., Deng, P., Ruan, Y. and Xu, Z. C. (2008) Dopamine D1-like receptors depress
  • excitatory synaptic transmissions in striatal neurons after transient forebrain ischemia. Stroke 39: 2370-2376 .
  • Lei, Z., Deng, P. and Xu, Z. C. (2008) Regulation of Kv4.2 channels by glutamate in cultured hippocampal neurons. J. Neurochem. 106: 182-192.
  • Fan, Y., Deng, P., Wang, Y., Lu, H., Xu, Z. C. and Schulz, P. E. (2008) Transient cerebral ischemia increases CA1 pyramidal neurons excitability. Exp. Neurol. 212:415-21.
  • Ruan, Y., Lei, Z., Fan, Y., Zou, B. and Xu, ZC. (2009) Diversity and Fluctuation of spine morphology in CA1 pyramidal neurons after transient global ischemia. J. Neurosci. Res, 87:61-68.
  • Li, Y., Lei, ZG and Xu, Z.C. (2009) Enhancement of inhibitory synaptic transmission in large aspiny neurons after transient cerebral ischemia. Neurosci. 159: 670-681.
  • Liang, R., Pang, ZP., Deng, P. and Xu, ZC. (2009) Transient enhancement of inhibitory synaptic transmission in hippocampal CA1 pyramidal neurons after cerebral ischemia. Neurosci. 160:412-418.
  • Deng, P., Pang, ZP., Lei, Z. and Xu, ZC (2009) Excitatory Roles of Protein Kinase C in Striatal Cholinergic Interneurons. J. Neurophysiol. 102:2453-2461.
  • Xu, H., He, M., Pang, X., Xu, ZC., Piesman, J. and Yang, XF. (2010) Characterization of the highly regulated antigen BBA05 in the enzootic cycle of Borrelia burgdorferi. Infection and Immunity 78:100-109.
  • Lei, Z., Deng, P., Li, Y. and Xu, ZC (2010) Down regulation of Kv4.2 channels mediated by NR2B-containing NMDA receptors in cultured hippocampal neurons. Neurosci. 165:350-362.
  • Liao, W.P., Shi, Y. W., Long Y. S., Zeng, Y., Li, T., Yu, M. J., Su, T., Deng, P., Lei, Z., Xu S. J., Deng, W. Y., Liu X. R., Sun W. W., Yi, Y. H, Xu, Z. C. and Duan S. (2010) Partial epilepsy with antecedent febrile seizures and seizure aggravation by antiepileptic drugs: Associated with loss of function of NaV 1.1. Epilepsia 51(9): 1669-78.
  • Li, Y., Blanco, G., Lei, Z., and Xu, Z. C. (2010) Increased GAD expression in the striatum after transient cerebral ischemia.  Molecular and Cellular Neurosci 45:370-377.
  • Deng, P. and Xu, Z. C. (2011) Contribution of Ih to neuronal damage in the hippocampus after traumatic brain injury.  J. Neurotrauma.  28(7): 1173-1183.
  • Deng, P., Pang, ZP., Lei, Z., Shikano, S., Xiong, Q., Harvey, B., London, B., Wang, Y., Li, M. and Xu, Z. C. (2011) Up-regulation of A-type potassium currents protects neurons against cerebral ischemia.  JCBFM 31: 1823-1835. Feature Article
  • Gao, X., Deng, P., Xu, Z. C., and Chen J. (2011) Moderate traumatic brain injury causes acute dendritic and synaptic degeneration in the hippocampal dentate gyrus. PLoS One. 6(9) e24566.
  • Lei, Z., Deng, P., Li, J. and Xu, Z. C. (2012) Alterations of A-type potassium channels in hippocampal neurons after traumatic brain injury.  J Neurotrauma. 29: 235-245.
  • Ruan, Y., Han, X., Shi, Z., Lei, Z. and Xu, Z. C. (2012) Remodeling of synapses in the CA1 area of the hippocampus after transient global ischemia. Neurosci. 218: 268-277.
  • Deng, L., Deng, P., Ruan, Y., Xu, Z. C., Liu, N., Smith, G. and Xu, X. M. (2013) A Novel Growth-Promoting Pathway Formed by GDNF-Overexpressing Schwann Cells Promotes Propriospinal Axonal Regeneration, Synapse formation, and Partial Recovery of Function after Spinal Cord Injury.  J. Neurosci. 33:5655–5667.
  • Lei, Z., Zhang, H., Liang, Y., Cui, Q., Xu, Z. and Xu, Z. C. (2014) Reduced expression of IA channels is associated with post-ischemic seizures in hyperglycemic rats.  J. Neurosci Res. 92:1775–1784.
  • Liang, Y., Lei, Z., Zhang, H., Xu, Z., Cui, Q. and Xu, Z.C. (2014) Toll-like receptor 4 is associated with seizures following ischemia with hyperglycemia. Brain Res. 1590: 75-84.

Department of Anatomy & Cell Biology | IU School of Medicine | 635 Barnhill Drive, MS 5035 | Indianapolis, IN 46202 | (317) 274-7494