Assistant Professional Researcher, Department of Oral and Maxillofacial Surgery, University of California, San Francisco, CA, USA
Assistant Professional Researcher, Department of Oral and Maxillofacial Surgery, University of California, San Francisco, CA, USA.
While I was trained as a medical student in China, I became more and more interested in the complexity of nervous system. That is why I switched to neuroscience research focusing on pain instead of working as a clinical doctor when I got my M.D degree.
In order to get better research training I came to University of California San Francisco (UCSF), a world-renowned institute for neuroscience research. I started as a postdoctoral fellow and now I work as an Assistant Professional Researcher in Department of Oral and Maxillofacial Surgery. My main research interests focus on the changes of glutamate receptors in sensory ganglia (dorsal root ganglia or trigeminal ganglia) in different pain situation like neuropathic pain, opioid induced hyperalgesia and migraine. We combine multiple methods like electrophysiology, immunohistology, molecular biology, animal behaviors etc to explore the plasticity of glutamate transmission system in pain situation.
1. Pain induced synaptic plastic changes in brain cortex
Latest concepts define that pain is not simply a sensation, and it also includes affection, emotion etc. Therefore, the high order of nervous system, such as brain cortex, is also involved in pain. Evidence from functional brain imaging studies has found that several brain regions, such as the primary somatosensory (S1), anterior cingular cortex (ACC), and hippocampus were activated in the process of pain. But it remains unclear how these brain cortices are involved. We think pain, especially pathological pain, can cause the changes of the neural activities in the brain, while the changes of synaptic plasticity are the bases of all these changes. And these might be the functional foundation for the affection or cognitional symptoms of pain. We found the activation of pyramidal neurons in brain cortex following pain stimulus. And this can be attributed to the imbalance between excitatory synaptic and inhibitory transmission. Recent studies found astrocytes in ACC could be activated by pain, and it is also known that there are GABA (gamma-aminobutyric acid) transporters (GATs) in astrocytes. I suspect these changes might contribute to the loss of inhibitory transmission after pain. By studying the synaptic changes caused by pain, we can contribute to understanding the pain mechanisms, thus helping us to control pain.
2. Cross talk between neuron and satellite glial cells in sensory ganglia.
Numerous studies have shown that there has been activation of satellite glial cells (SGCs) in DRG in the pain condition. According to our past studies, we have found that the activation of Dorsal root ganglion (DRG) neurons driven by dorsal root reflex (DRRs) is pivotal for the neurons to release the inflammatory factors. And it is also well established that neurogenic inflammation contributed a lot to the development of the chronic painful status like arthritis, migraine, etc. However, it remains less well studied that whether SGCs could modulate the development of neurogenic inflammation in this situation and how SGCs modulates the process. We are interested in the crosstalk between neurons and SGCs in pain situations. We suspect that SGCs might produce some cytokines (such as TNF alph, CCL2) to participate in the neurogenic inflammation. The mechanisms how neurons transmitted the information to SGCs, and how these cytokines affect DRG neurons remain to be studied.
3. Contribution of peripheral glutamate in nociception
The important role of glutamate in neurotransmission has been well recognized for pain. However, it remains largely unclear whether glutamate in peripheral sites like sensory ganglia, is involved in nociception. By combining multiple techniques like immunohistology and electrophysiology, we identified that glutamate is an important neurotransmitter in the sensory ganglia and also plays critical roles in nociception. For example, upregulated glutamate receptors were identified in DRG neurons in neuropathic pain and opioid induced hyperalgesia. But it is still unknown whether glutamate could be released from DRG neuron soma. We are using virus mediated fluorescent glutamate receptors and electrophysiology to how glutamate is released from neuron soma. We will also observe whether the ability of releasing glutamate can be strengthened in pain situation.