Hui-Chen Lui

Hui-Chen Lui

Professor, Psychological and Brain Sciences

Linda and Jack Gill Chair, Neuroscience

  • (812) 856-9663
  • Multidisciplinary Science Building II 122
  • Office Hours


  • Postdoctoral Fellow, Baylor College of Medicine, 1997-2003
  • Ph.D., Baylor College of Medicine, 1997
  • B.S., National Taiwan University, 1991


  • Development of neural circuitry, particularly in the neocortex
  • Activity-dependent remodeling and mis-wiring in autism, dyslexia, schizophrenia, and 
    congenital epilepsy
  • Neuroprotective strategies

    Mis-wiring of neuronal circuits during early life is likely to be a major cause of neurological disorders, including autism and schizophrenia. The Lu lab is intersted in how activity-dependent processes during brain development fine-tune the establishment of neural circuits and how sensory experiences affect neural circuit wiring and cognitive behaviors. Specifically, we are interested in exploring the role of the metabotropic glutamate receptor 5 (mGluR5), a group 1 metabotropic glutamate receptor. mGluR5 mutations have been identified in some ADHD and schizophrenic patients. We employ mouse genetic tools to understand the contribution of mGluR5 signaling in specific neuronal populations to sensory circuit formation, synaptic function/plasticity, and behavior. We are also exploring the role of the endogenous cannabinoid (endocannabinoid) system in fetal brain development and investigating how prenatal cannabis exposure affects brain development and later behaviors. Understanding the effects of endocannabinoids during neural circuit formation will not only shed light on normal brain development and function but will also allow us to assess endocannabinoid-based therapies and the effects of cannabis use on the developing fetus.

    Proper brain function requires an active maintenance program to sustain neuronal health. Environmental stressors detrimentally impact the nervous system, predisposing it to neuronal dysfunction and degeneration if neuroprotective mechanisms are weakened. Recent studies by others and us revealed that NMNAT2 (nicotinamide mononucleotide adenylyl transferase 2) is a neuroprotective protein that is central to maintain neuronal integrity and facilitate proper neural function throughout life. NMNAT2 abundance is significantly reduced in Alzheimer’s Disease (AD) brains. Increasing Nmnat2 expression in neurodegenerative animal models reduced neurodegeneration.  We hope to elucidate the mechanisms underlying NMNAT2’s neuroprotection and how NMNAT2 expression is down-regulated in pathological conditions.  In addition, we hope to develop NMNAT2-specific therapies to prevent or reduce neurodegeneration.