Profile
Qingchun Tong, Ph.D.
Click here for a permanent link to this profileAssistant Professor Center for Obesity and Diabetes
(713) 500-3453
To tackle the complexity in the hypothalamic neural network in the regulation of energy balance, Dr. Tong's group will generate mouse models with gene-deletion restricted to defined groups of brain neurons using Cre-loxP technology. Using these animal models, as well as an array of techniques including immunohistochemistry, in situ hybridization, neuronal tracing and stereotaxic delivery, his group will try to delineate neural pathways in the brain underlying food intake, body weight homeostasis and glucose homeostasis, and provide a framework for an efficient drug design against the current epidemics of obesity and its associated syndromes.
Dr. Tong obtained his B.S. degree in Biology from Anhui Normal University in China in 1996. Immediately after that, he managed to get enrolled in one of most prestigious research institutes in China: Shanghai Institute of Physiology, Chinese Academy of Sciences, and there he got his master degree in Physiology in 1999. To get a better training and education, Dr. Tong then went to State University of New York Downstate Medical Center for his PhD training. He studied the role of glutamatergic neurotransmission in the enteric nervous system and in the pancreatic islets. When his PhD training was near end, he became fascinated by the fast growing field in the central control of obesity and diabetes. At the same time, he was surprised by the fact that the role of the fast-acting neurotransmitters (glutamate and GABA), as the major communicator between neurons, has not been critically examined. The majority, if not all, neurons in the brain release either glutamate or GABA (glycine), and almost every neuron in the brain expresses their receptors. Therefore, understanding the function of glutamate and GABA release is a prerequisite to understand mechanisms in the regulation of energy balance. With this mind, after completion of his PhD study in 2003, Dr. Tong moved to Beth Israel Deaconess Medical Center and Harvard Medical School working with Drs. Brad Lowell and Joel Elmquist, the renowned experts in the central control of energy balance. At Harvard, Dr. Tong successfully initiated a new line of research toward understanding the roles of glutamate and GABA release in hypothalamic neurocircuitry controlling energy balance. He has generated a few interesting models in which glutamate or GABA release is disrupted only from a restricted group of neurons in the hypothalamus, and found the fast-acting neurotransmitters are required for normal regulation of energy balance.
In 2009, Dr. Tong started his own lab in the Center for Diabetes and Obesity Research, Institute of Molecular Medicine of the University of Texas Health Science Center at Houston, where he will continue to investigate the role of fast-acting neurotransmitters from novel groups of hypothalamic neurons. In addition, he will extend this line of research by generating mice with inducible region-specific disruption of glutamate or GABA release to investigate the role of these neurotransmitters in the adult state without a potential compensation. By using tracing studies and animal surgeries on these animal models, specific neural pathways underlying specific physiologic functions (body weight, glucose homeostasis, etc.) will also be investigated.
Honors
Pilot and Feasibility Award, Boston Area Diabetes and Endocrinology Research Center (BADERC). 2009
Pilot and Feasibility Award, Boston Obesity and Nutrition Research Center (BONRC) 2007
Young Investigator Award, NAASO 2007
Keystone Symposia Travel Scholarship Award 2007
Research Interests:
Obesity and its associated complications are imposing a huge burden on our society, while its effective treatment is still lacking. A better understanding of the mechanisms regulating energy balance is required to develop new therapeutic strategies. Neurons in the hypothalamus receive and integrate nutritional status signals, and then adjust food intake and energy expenditure accordingly to maintain energy balance. Previous research has identified important functions of a few groups of hypothalamic neurons (e.g. POMC neurons, AgRP neurons, etc.) and a few hypothalamic genes (POMC, AgRP and MC4R, etc.). However, the mechanisms with which the hypothalamus regulates energy balance are not well understood.
The research focus of my group is to understand how neurocircuitry in the hypothalamus regulates energy balance. My current research focus is to understand the role of glutamate and GABA release from hypothalamic neurons in the regulation of energy balance. Glutamate and GABA are the main excitatory and inhibitory neurotransmitters, respectively, in the brain. However, research efforts that address the mechanisms underlying energy balance have been largely focusing on the roles of neuropeptides, while the roles of glutamate and GABA have been overlooked. To study the roles of glutamate and GABA release, we generated mice with floxed vesicular glutamate transporter 2 (Vglut2, required for presynaptic glutamate release in the hypothalamus) and floxed vesicular GABA transporter (Vgat, required for presynaptic GABA release). These mice will be crossed with transgenic mouse lines that express Cre only in a subset of hypothalamic neurons to generate mice with disruption of glutamate (lox-Vglut2) or GABA (lox-Vgat) release only from the Cre-expressing neurons. These models will then be used to study the function of neural pathways in which these glutamatergic or GABAergic neurons engage to regulate energy balance. Ultimately we try to delineate specific neural pathways underlying specific physiologic functions.
Publications:
- Vetrivelan R, Fuller P, Tong Q. and Lu J. Medullary circuitry regulating rapid eye movement (REM) sleep and motor atonia. J Neurosci., 2009, in press.
- Tong Q, Ye C, Jones JE, Elmquist JK and Lowell BB. Synatpic GABA Release by AgRP neurons is Required for Normal Regulation of Energy Balance. Nature Neuroscience 11:998-1000, 2008.
- Tong Q, Ye C, McCrimmon RJ, Dhillon H, Choi B, Kramer MD, Yu J, Yang Z, Christiansen LM, Lee CE, Choi CS, Zigman JM, Shulman GI, Sherwin RS, Elmquist JK and Lowell BB. Synaptic Glutamate Release by Ventromedial Hypothalamic Neurons is Part of the Neurocircuitry that Prevents Hypoglycemia. Cell Metabolism 5(5):383-393, 2007.
- Tong Q and Kirchgessner A. Localization and Function of metabotropic glutamate receptor 8 in the Enteric Nervous System. American Journal of Physiology 285: G992-G1003, 2003.
- Tong Q, Ouderaogo R and Kirchgessner A. Localization and Function of Group III Metabotropic Glutamate Receptors in Rat Pancreatic Islets. American Journal of Physiology 282:E1324-E1333, 2002.
- Tong Q, Ma J and Kirchgessner A. Vesicular Glutamate Transporter 2 in the Brain-gut Axis. NeuroReport 12(18): 3929-3934, 2001.
- Xu Y, Wu J, Pei J, Shi Y, Ji Y and Tong Q. Solution Structure of BmP02, a New Potassium Channel Blocker from the Venom of the Chinese Scorpion Buthus martensi Karsch. Biochemistry 39(45): 13669-13675, 2000.
- Tong Q, Zhang Y, Li DP, Zhou ZN and Ji Y. The Blocking Effects of BmP02, One Novel Short-chain Scorpion Peptide On Transient Outward K+ Channel of Adult Rat Ventricular Myocyte. Regulatory Peptide 90(1-3): 85-92, 2000.
- Tong Q, Zhang Y, Zhou ZN and Ji Y. The Characterizations and Blocking Effects On Ito of Rat Ventricular Myocyte of New Minipeptides From Buthus martensi Karsch. Acta Biochimica et Biophysica Sinica 31(3): 347-349, 1999.