Department of Anesthesiology/Critical Care Medicine
The Johns Hopkins University School of Medicine
720 Rutland Avenue, 370 Ross
Baltimore, MD 21205
Chronic or persistent pain is one of the most common syndromes among clinical disorders and affects 26 million people worldwide—10 million in the United States alone. Chronic pain may result from inflammation, tissue injury, and nerve injury. It is characterized by spontaneous, ongoing or intermittent burning pain, an exaggerated response to painful stimuli, and pain in response to normally innocuous stimuli. Despite intensive research into the neurobiologic mechanism of chronic pain during the past decades, our understanding of chronic pain is still in its infancy, and its treatment is often poorly managed by current drugs such as opioids and nonsteroidal anti-inflammatory drugs. Accordingly, further understanding molecular and cellular mechanisms of chronic pain is critical for improving clinical treatment and developing novel therapeutic strategies.
The research projects in Dr. Tao’s laboratory focus on molecular and cellular mechanisms that underlie central sensitization of chronic pain. Dr. Tao and his colleagues have identified the role of spinal cord synaptic scaffolding proteins (e.g., PSD-95 and PSD-93) in the development and maintenance of chronic inflammatory and neuropathic pain. Their recent publications reported that these synaptic scaffolding proteins both cluster and target the glutamate receptors at synapses and participate in synaptic receptor trafficking in dorsal horn neurons under chronic pain conditions. Ongoing projects study whether and how peripheral noxious insults lead to spinal glutamate receptor trafficking and whether this trafficking contributes to central mechanisms of chronic pain. The analytical methodology includes molecular biology, immunocytochemistry, biochemistry, transmission electron microscopy, electrophysiology, and pain behavioral tests.
Defining these underlying mechanisms of chronic pain could greatly increase our knowledge in this area and perhaps identify targets for mitigating persistent pain conditions.
- American Society of Pain
- International Society for the Study of Pain
- Society of Neuroscience
- Liaw W-J, Stephens RL Jr, Binns BC, Chu Y, Sepkuty J, Johns RA, Rothstein JD, Tao YX. Spinal glutamate uptake is critical for maintianing normal sensory transmission in rat spinal cord. Pain 115:60–70, 2005.
- Chu YC, Guan Y, Skinner J, Raja SN, Johns RA, Tao YX. Effect of genetic knockout or pharmacologic inhibition of neuronal nitric oxide synthase on complete Freund's adjuvant-induced persistent pain. Pain 119:113–23, 2005.
- Liaw W-J, Zhu X-G, Yaster M, Johns RA, Gauda EB, Tao YX. Distinct expression of synaptic NR2A and NR2B in the central nervous system and impaired morphine tolerance and physical dependence in mice deficient in postsynaptic density-93 protein. Mol Pain 4:45, 2008.
- Singh OV, Yaster M, Guan Y, Dharmarajan AM, Raja SN, Zeitlin PL, Tao YX. Proteome of synaptosome-associated proteins in spinal cord dorsal horn after peripheral nerve injury. Proteomics 9 1241–53, 2009.
- Park J-S, Voitenko N, Petralia RS., Guan X, Xu JT, Steinberg JP, Talamiya K, Sotnik A, Kopach O, Huganir RL, Tao YX. Persistent inflammation induces GluR2 internalization via NMDA receptor-triggered PKC activation in dorsal horn neurons. J Neurosci 29:3206-19, 2009.
- Tao YX. Dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor trafficking in inflammatory pain. Anesthesiology 112:1259-65, 2010.
Laboratory Members/Key Associates
Fidelis E. Atianjoh, PhD
Lingli Liang, MD, PhD
Vinod Tiwarim, PhD
Yong Zhang, PhD
Jianyuan Zhao, PhD
Longcheng Fan, MD, PhD
Jin-Bian Liiu, MD, PhD
A prize for a remarkable contribution to Nature and Science from Chinese Academy of Sciences in 1999