Hui Zhang, PhD

Assistant Professor, Department of Neuroscience
Vickie and Jack Farber Institute for Neurosciences

Zhang, Hui

Contact

900 Walnut Street
JHN 4th floor
Philadelphia, PA 19107

Email Hui Zhang

215-503-7213
215-503-4358 fax

Hui Zhang, PhD

Assistant Professor, Department of Neuroscience
Vickie and Jack Farber Institute for Neurosciences

Expertise and Research Interests

Research in my laboratory aims to elucidate the pathogenic mechanisms of Parkinson's disease and Schizophrenia at the molecular, cellular and synaptic levels. Much effort is directed at the striatum, the input nucleus of the basal ganglia and the prefrontal cortex, a cortical region which plays a central role in cognition. We employ a combination of electrochemical, electrophysiological, optical imaging, optogenetics, and genetic approaches to explore the plasticity of dopamine neurotransmission, the role of dopamine in modulating information flow and how the process is disturbed in these disorders. In addition, we are developing optical tools to study whether dopamine dys-regulation in schizophrenia is in part due to intrinsic changes in the presynaptic dopamine terminals.

Publications

Current Projects

  • The pathophysiology of Parkinson's disease: LRRK2 mediated pathogenic pathways in dopaminergic axonal degeneration and synaptic transmission 
  • Dopamine neurotransmission and modulation of the prefrontal cortex in mouse models of schizophrenia 
  • The role of tonic and phasic dopamine signaling in the striatum

Most Recent Peer-Reviewed Publications

 

  1. Vitamin B 12 modulates Parkinson’s disease LRRK2 kinase activity through allosteric regulation and confers neuroprotection
  2. Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction
  3. LRRK2 and mitochondria: Recent advances and current views
  4. A schizophrenia-related deletion leads to KCNQ2-dependent abnormal dopaminergic modulation of prefrontal cortical interneuron activity
  5. Effects of LRRK2 Inhibitors on Nigrostriatal Dopaminergic Neurotransmission
  6. Loss of VGLUT3 produces circadian-dependent hyperdopaminergia and ameliorates motor dysfunction and l-dopa-mediated dyskinesias in a model of parkinson’s disease
  7. Fluorescent dopamine tracer resolves individual dopaminergic synapses and their activity in the brain
  8. Vesicular Glutamate Transport Promotes Dopamine Storage and Glutamate Corelease In Vivo
  9. Fluorescent false neurotransmitters visualize dopamine release from individual presynaptic terminals
  10. Dopamine release at individual presynaptic terminals visualized with FFNs
  11. Repeated Exposure to Methamphetamine Causes Long-Lasting Presynaptic Corticostriatal Depression that Is Renormalized with Drug Readministration
  12. Transcriptional and behavioral interaction between 22q11.2 orthologs modulates schizophrenia-related phenotypes in mice
  13. Neurotoxicity and behavioral deficits associated with Septin 5 accumulation in dopaminergic neurons
  14. Frequency-dependent modulation of dopamine release by nicotine
  15. Heterosynaptic dopamine neurotransmission selects sets of corticostriatal terminals
  16. Erratum: Real-time decoding of dopamine concentration changes in the caudate-putamen during tonic and phasic firing (Journal of Neurochemistry (2003) 87 (1284-1295))
  17. Regulation of the Development of Mesencephalic Dopaminergic Systems by the Selective Expression of Glial Cell Line-Derived Neurotrophic Factor in Their Targets
  18. Dopamine Neurons Mediate a Fast Excitatory Signal via Their Glutamatergic Synapses
  19. Real-time decoding of dopamine concentration changes in the caudate-putamen during tonic and phasic firing
  20. Glutamate Spillover in the Striatum Depresses Dopaminergic Transmission by Activating Group I Metabotropic Glutamate Receptors