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Zao C. Xu, M.D., Ph.D.

Professor of Anatomy and Cell Biology

Education/ Training:
M.D., Guangzhou Medical College (1982)
Ph.D., University of Tennessee, Memphis (1990)


Alternation of neuronal excitability in neurological disorders.

Excitotoxicity is the major cuase 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.  The research in my lab is to reveal the role of alteration of neuronal excitability in pathogenesis of neurological disorders.  The current projects in my lab:

  1. Stroke is the leading cause of dead and disability in U.S.. Transient cerebral ischemia results in seletive 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 model of transient global ischemia and oxygen-glucose deprivation model of neuronal culture with electrophysiological and molecular biological approaches.
  2. Seizure/epilepsy is a common sequal of acute neurological disorders including traumatic brain injury.  In addition to study the excitablity change after TBI that might contribute post traumatic epilepsy (PTE), we also investigate the possible role of inflammation factors in PTE using animal model and patients data.

Search for Dr. Xu on PubMed

Recent Publications:

  1. 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.

  2. 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 with commentary

  3. 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.

  4. 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.

  5. 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.

  6. 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.

  7. 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. (In press).

  8. Liang Y, Lei Z, Zhang H, Xu Z, Cui Q, and Xu ZC. (2014) Toll-like receptor 4 is associated with seizures following ischemia with hyperglycemia. Brain Res. 1590: 75-84.

Stark Neurosciences Research Institute | Neuroscience Research Building | 320 West 15th Street | Indianapolis, IN 46202 | Phone: (317) 278-5848 | FAX: (317) 231-0203