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Jun Wang, PhD

Jun Wang
Jun Wang, PhD

Associate Professor

Contact

Department of Neuroscience & Experimental Therapeutics
8447 Riverside Pkwy
2106 Medical Research and Education Building
Bryan , TX 77807
jwang188@tamu.edu
Phone: 979.436.0389
Fax: 979.436.0086
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Wang Lab

Education and Training

  • Tongji Medical University, MD
  • Shanghai Brain Research Institute, Chinese Academy of Sciences, PhD
  • University of California at Berkeley and at San Francisco, Postdoctoral Fellow

Research Interests

  • The Wang lab's research focuses on the role of basal ganglia circuitry in the neurobiological basis of neuropsychiatric diseases. These diseases include alcohol use disorder (alcohol addiction), opioid use disorder, and Alzheimer's.
  • The dorsal striatum of the basal ganglia circuity. The dorsal striatum, a main entry of the basal ganglia, is divided into the dorsomedial (DMS) and dorsolateral (DLS) striatum. The DMS mediates goal-directed behaviors, and the DMS controls habit learning. The DMS receives excitatory inputs from the cortex (e.g., the medial prefrontal cortex) and thalamus (e.g., the parafascicular nucleus or PfN). The striatum contains principal medium spiny neurons (MSNs) and cholinergic interneurons (CINs). Dopamine D1 receptor-expressing MSNs (D1R-MSNs or dMSNs) project to the substantia nigra pars reticulata (SNr) and entopeduncular nucleus (EP), giving rise to the direct pathway. D2R-expressing MSNs (D2R-MSNs or iMSNs) project to the internal globus pallidus (GPe), which, in turn, innervates the SNr and EP, forming the indirect pathway.
  • Synaptic plasticity and alcohol use disorder. The Wang lab is interested in exploring alcohol-induced input (the mPFC versus amygdala)- and cell type (dMSNs versus iMSNs)-specific plasticity in the DMS. Using a combination of slice electrophysiology, optogenetics, viral and animal transgenics, and FosTRAP approaches, the Wang group investigates how alcohol self-administration causes synapse-specific aberrant plasticity in DMS neuronal ensembles and how these synaptic alterations are involved in pathological drinking. In addition, the few available medications for alcoholism often fail to prevent relapse to alcohol, perhaps because they do not reverse the alcohol-evoked long-term synaptic plasticity, which likely drives alcohol seeking and relapse. The Wang lab employs dual-channel optogenetics to normalize the alcohol-induced circuit-specific plasticity, thereby persistently reducing alcohol seeking and relapse in operant self-administration. They express two excitatory rhodopsins, Chrons and Chrimson, in the presynaptic terminals and postsynaptic MSNs and activate them using blue and yellow light, respectively. They then induce long-term potentiation (LTP) or depression (LTD) in vivo using optogenetic high-frequency stimulation (HFS) or spike-timing-dependent protocols (STDP) to change animal-seeking and relapsing behavior persistently.
  • Cognitive flexibility and alcohol use disorder. The Wang lab is also interested in elucidating the mechanism of compulsive inflexible drinking. They study how pathological drinking alters thalamic PfN-->CIN activity in reversal learning of instrumental action-outcome contingency, and how the drinking alters CIN-mediated regulation of corticostriatal transmission in dMSNs and iMSNs. The results of the alcohol research will guide future efforts toward the development of more effective therapeutics for alcohol use disorders.
  • Striatal patch versus matrix compartments and opioid use disorder. The striatal patch (striosome) compartment contains extensive mu-opioid receptors (MORs). The Wang lab investigates how MOR-expressing MSNs, the non-motor outputs of the basal ganglia (i.e., EP), their downstream circuit (i.e., the lateral habenula), contributes to opioid use disorder, with a particular interest in fentanyl abuse.
  • Motor deficits in Alzheimer's disease. Human MRI studies found Aβ deficits in the striatum of Alzheimer's patients who showed motor-related deficits. The Wang lab explores how corticostriatal transmission in MSNs, CIN activity, and cholinergic neuron activity in the basal forebrain are altered in the 5xFAD mouse model of Alzheimer's disease. They are also interested in how alcohol drinking exacerbates these alterations.
  • Dr. Wang participates in graduate training as a faculty member in the Medical Science Ph.D. program in the College of Medicine, the Interdisciplinary Program in Neuroscience (TAMIN), and the Interdisciplinary Toxicology Program.

Representative Publications

Complete Bibiliography on NCBI

  • Wei Wang, Xueyi Xie, Xiaowen Zhuang, Yufei Huang, Tao Tan, Himanshu Gangal, Zhenbo Huang, William Purvines, Xuehua Wang, Alexander Stefanov, Ruifeng Chen, Emily Yu, Michelle Hook, Yun Huang, Emmanuel Darcq, and Jun Wang. Striatal Mu-Opioid Receptor Activation Triggers Direct-Pathway GABAergic Plasticity to Induce Negative Affect. BioRxiv (2022).
  • Tengfei Ma, Zhenbo Huang, Xueyi Xie, Xiaowen Zhuang, Matthew Childs, Himanshu Gangal, Xuehua Wang, Laura N Smith, Rachel J Smith, Yubin Zhou, and Jun Wang. Chronic alcohol drinking persistently suppresses thalamostriatal excitation of cholinergic neurons to impair cognitive flexibility. The Journal of Clinical Investigation, 2021, doi:10.1172/JCI154969 (2021).
  • Yifeng Cheng, Xueyi Xie, Jiayi Lu, Himanshu Gangal, Wei Wang, Sebastian Melo, Xuehua Wang, Jared Jerger, Kayla Woodson, Eric Garr, Yufei Huang, Patricia Janak, Jun Wang. Optogenetic induction of orbitostriatal long-term potentiation in the dorsomedial striatum elicits a persistent reduction of alcohol-seeking behavior in rats. Neuropharmacology 191:108560 (2021).
  • Jiayi Lu, Yifeng Cheng, Xueyi Xie, Kayla Woodson, Jordan Bonifacio, Emily Disney, Britton Barbee, Xuehua Wang, Marian Zaidi, Jun Wang. Whole-brain mapping of direct inputs to dopamine D1 and D2 receptor-expressing medium spiny neurons in the posterior dorsomedial striatum. eNeuro, 8:0348-0320.2020.
  • Jiayi Lu, Yifeng Cheng, Xuehua Wang, Kayla Woodson, Craig Kemper, Emily Disney, and Jun Wang. Alcohol Intake Enhances Glutamatergic Transmission from D2 Receptor-Expressing Afferents onto D1 Receptor-Expressing Medium Spiny Neurons in the Dorsomedial Striatum. Neuropsychopharmacology, 44:1123-1131 (2019).
  • Yifeng Cheng and Jun Wang. The Use of Chemogenetic Approaches in Alcohol Use Disorder Research and Treatment. Alcohol, 74:39-45 (2019).
  • Yifeng Cheng, Xuehua Wang, Xiaoyan Wei, Xueyi Xie, Sebastian Melo, Rajesh C. Miranda, and Jun Wang. Prenatal Exposure to Alcohol Induces Functional and Structural Plasticity in Dopamine D1 Receptor-Expressing Neurons of the Dorsomedial Striatum.
    Alcoholism: Clinical and Experimental Research Research, 42:1493-1502 (2018).
  • Tengfei Ma#, Yifeng Cheng#, Emily Roltsch Hellard, Xuehua Wang, Jiayi Lu, Xinsheng Gao, Cathy C.Y. Huang, Xiao-Yan Wei, Jun-Yuan Ji, and Jun Wang. Bidirectional and Long-Lasting Control of Alcohol-Seeking Behavior by Corticostriatal LTP and LTD. Nature Neuroscience, 21:373-383 (2018).
    This article was recommended in Faculty of 1000 as being of special significance in its field: https://f1000.com/prime/732647279).
  • Xiaoyan, Wei#, Tengfei Ma#, Yifeng Cheng, Cathy C.Y. Huang, Xuehua Wang, Jiayi Lu, and Jun Wang. Dopamine D1 or D2 Receptor-Expressing Neurons in the Central Nervous System. Addiction Biology, 23:569-584 (2017). (#Equal contribution)
  • Cathy C.Y. Huang#, Tengfei Ma#, Emily Roltsch Hellard#, Xuehua Wang, Amutha Selvamani, Jiayi Lu, Farida Sohrabji, and Jun Wang. Stroke Triggers Nigrostriatal Plasticity and Increases Alcohol Consumption in Rats. Scientific Reports, 7:2501 (2017).
  • Tengfei Ma, Britton Barbee, Xuehua Wang, and Jun Wang. Alcohol Induces Input-Specific Aberrant Synaptic Plasticity in the Rat Dorsomedial Striatum. Neuropharmacology, 123: 46-54 (2017).
  • Yifeng Cheng#, Cathy C.Y. Huang#, Tengfei Ma#, Xiaoyan Wei, Xuehua Wang, Jiayi Lu, and Jun Wang*. Distinct Synaptic Strengthening of the Striatal Direct and Indirect Pathways Drives Alcohol Consumption. Biological Psychiatry, 81: 918-929 (2017).
    Figure 1A of this article was selected for the cover page of this issue.
    This article was highlighted "In This Issue" section.
    This article received a Commentary "Tipping Scales Toward Addiction", 81: 903-904 (2017).
  • Jun Wang*, Yifeng Cheng, Xuehua Wang, Emily Roltsch, Tengfei Ma, Hannah Gil, Sami Ben Hamida, and Dorit Ron*. Alcohol Elicits Functional and Structural Plasticity Selectively in Dopamine D1 Receptor-Expressing Neurons of the Dorsomedial Striatum. Journal of Neuroscience 35: 11634-11643 (2015). *Corresponding authors.
    This article was highlighted in the "This Week in The Journal" section.
  • Jun Wang, Sami Ben Hamida, Emmanuel Darcq, Wenheng Zhu, Stuart L. Gibb, Maria Fe Lanfranco, Sebastien Carnicella, and Dorit Ron. Ethanol-Mediated Facilitation of AMPA Receptor Function in the Dorsomedial Striatum: Implication for Alcohol Drinking Behavior. The Journal of Neuroscience 32:15124 –15132 (2012).
  • Jun Wang, Maria Fe Lanfranco, Stuart L. Gibb, Quinn V. Yowell, Sebastien Carnicella, and Dorit Ron. Long-Lasting Adaptations of the NR2B-Containing NMDA Receptors in the Dorsomedial Striatum Play a Crucial Role in Alcohol Consumption and Relapse. The Journal of Neuroscience 30:10187-10198 (2010a).
  • Jun Wang, Sebastien Carnicella, Dao-Yao He, Somayeh Ahmadiantehrani, Segev Barak, Sami Ben Hamida, Viktor Kharazia, Agustin Zapata, Toni S. Shippenberg, and Dorit Ron. Nucleus Accumbens-Derived GDNF Is a Retrograde Enhancer of Dopaminergic Tone in the Mesocorticolimbic System. The Journal of Neuroscience 30: 14502-14512, (2010b).
  • Jun Wang, Sebastien Carnicella, Khanhky Phamluong, Jerome Jeanblanc, Jennifer A. Ronesi, Nadia Chaudhri, Patricia H. Janak, David M. Lovinger, and Dorit Ron. Ethanol Induces Long-Term Facilitation of NR2B-NMDA Receptor Activity in the Dorsal Striatum: Implications for Alcohol Drinking Behavior. The Journal of Neuroscience27:3593-3602 (2007). 
    (Faculty of 1000 Biology: http://www.f1000biology.com/article/id/1085799, factor 6 “must read” category).
  • Jorge J. Palop, Jeannie Chin, Erik D. Roberson, Jun Wang, Myo T. Thwin, Nga Bien-Ly, Jong Yoo, Kaitlyn O. Ho, Gui-Qiu Yu, Anatol Kreitzer, Steven Finkbeiner, Jeffrey L. Noebels, and Lennart Mucke. Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer’s Disease. Neuron 55:697-711 (2007).

Lab Members

  • Dr. Jun Wang – Principal Investigator
  • Dr. Tao Tan – Research Scientist
  • Dr. Zhenbo Huang – Postdoctoral fellow
  • Daisy Wang – Research Associate
  • Himanshu Gangal – PhD student (TAMIN)
  • Xueyi Xie – PhD student (College of Medicine)
  • Amanda Essoh – PhD student (College of Medicine)
  • William Purvine – PhD student (TAMIN)
  • Wei Wang – PhD student (Toxicology)
  • Yufei Huang – PhD student (TAMIN)
  • Ruifeng Chen – PhD student (Toxicology)
  • Claire Marshall – Research Student
  • Benjamin Henderson – Research Student
  • John Chainaranont – Research Student
  • John Carter – Research Student
  • Joanna Mendoza – Research Student
  • Matthew Childs – Research Student
  • Daniel Shi – Research Student

Trainees

  • Tengfei Ma – Nanjin Medical University
  • Cathy Huang – Taiwan Nationa Central University
  • Emily A. Roltsch Hellard – Former postdoctoral fellow
  • Xiaowen Zhuang – UCSF
  • Yifeng Cheng – John Hopkins University
  • Jiayi (Ada) Lu – UT Health Science Center at Houston
  • Annalise Binette – Texas A&M University
  • Sebastian Melo – Medical student, Texas A&M Health Science Center
  • Swetha Jayavelu – Medical student, UT Health Science Center at San Antonio
  • Xiaoyan Wei – The Fourth Military Medical University, China
  • Aggie Migut – Medical student, UT Health Science Center in Houston, 2015
  • Meagan Coner – Graduate Program in Neuroscience, Stony Brook University, 2016
  • Britton Barbee – Graduate Program in Molecular and Systems Pharmacology, Emory University, 2017
  • Chris Arp – Graduate Program in Chemistry, New York University, 2017
  • Bradely Jones  – Texas A&M Neuroscience Program 2017
  • Nathaniel Teplitskiy – Columbina University

Lab Phone: 979.436.0339