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Zhou, Feng C., PhD

Education

  • National Taiwan Normal University, Taipei, Taiwan, BS, 1975
  • Mount Sinai School of Medicine of City University of New York, MPh, 1982
  • Mount Sinai School of Medicine of City University of New York, PhD, 1983
  • New York University, Postdoctoral Fellowship, 1983-1985

 

Academic Appointments

  • 7/1983-7/1985 Assistant Professor of Anatomy, New York College, Podiatric Medicine
  • 8/1984-7/1987 Adjunct Assistant Professor of Biology, New York University
  • 7/1985-7/1987 Assistant Research-Anatomist, UCLA, School of Medicine
  • 7/1987-6/1991 Assistant Professor of Anatomy and Medical Neurobiology, Indiana Univ. Sch. Med.
  • 7/1991-6/1997 Associate Professor of Anatomy and Medical Neurobiology, tenured, Indiana Univ. Sch. Med.
  • 7/1997- Professor of Anatomy/ Cell Biology and Medical Neurobiology, Indiana Univ. Sch. Med.
  • 2/2009- Professor of Psychology, Indiana University Purdue University at Indianapolis

 

CV in PDF format     Lab Page    SNRI

My long-term research interests include the area of neural development and neural plasticity of the brain as well as related dysfunctions and diseases. In recent years, my team has focused on the neural program during development and its reprogramming responses to environmental inputs at a mature stage. We believe our brain is precisely shaped through a, intrinsic, yet-to-be explored, genetic-cellular expression that is orchestrated further upstream by an epigenetic program. This program can be influenced by environmental inputs such as alcohol and drugs. One central hypothesis we are working on is how orchestrated gene expressions are achieved through programs of DNA methylation, histone code modifications, and chromatin modeling. We are investigating how such orchestrated gene expression is programed by epigenetics during neural stem cell differentiation, how Fetal Alcohol Spectrum Disorder (FASD) is mediated through gene x environmental interaction, and how alcohol addiction, an altered state of the mind, is supported by a changing neurochemical program as well as epigenetics.

 

Neural Stem Cells: Neural stem cells are major building blocks of the brain during development and are implicated in the adult brain for depression.  They are also a potential source of repair after neurodegeneration, e.g. traumatic brain and spinal cord injury. We are studying the epigenetic program of neural stem cells that orchestrate the gene expression and cellular response from the quiescent state to active differentiation as well as their responses  to environmental insults. To accomplish this, we use an established bank of embryonic stem (ES) cells, embryonic neural stem cells, and adult neural stem cells from rodents and humans to model the development and repair of CNS. Significantly, we have demonstrated a DNA methylation program from the quiescent state to differentiation and are currently investigating its functionality.

Fetal Alcohol Spectrum Disorder: Women drinking during pregnancy can result in Fetal Alcohol Spectrum Disorder (FASD), which features neurodevelopmental deficit, microencephaly, facial dysmorphology, low IQ, and difficulties in social adaptation. Our study demonstrated that serotonin, dopamine, neural crest cells, and sensory cortical wiring become impaired. The mechanism, diagnosis, and the potential treatment of FASD are under current investigation. We have demonstrated alcohol altered epigenetic program, expressions of cohorts of neural specification genes, and cell cycling genes in the canonical developmental pathways, including bHLH, neurogenin and Ascl1.

Alcohol Abuse and Synaptic Adaptation: A family history of positive alcohol preference is likely to have both a genetic and epigenetic contributions. Using an alcohol preference rodent model (P/NP; HAD/LAD), we have demonstrated an innate difference of serotonin and dopamine between the lines. Further, repeated high alcohol intake can induce neuroadaptation to an altered state. We are investigating how chronic alcohol exposure induces the brain into an “addictive” state at a neurochemical and synaptic level. Under two-photon microscopy, we have demonstrated that alcohol alters the presynaptic glutamate and dopamine ratio and the postsynaptic NMDA as well as affecting AMPA receptors on the conformation and the number of dendritic spines in the reward circuitry. We are currently studying the epigenetic and genetic contributions to the gene expressions that underpin the neurochemical and neuroanatomical differences that, in turn, contribute to drinking behavior.

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