Department of Neuroscience, Cell Biology, & Anatomy
Room 2.143 Medical Research Building
: 1069 |
(409)772-6555 | Fax:
(409) 762-9382 | firstname.lastname@example.org
Education and Training
PhD in Biophysics, State University of New York at Buffalo
Post-Doctoral in Laboratory of Biophysics and Laboratory of Neurophysiology, NINDS, National Institutes of Health
Visiting Scientist in Department of Membrane Biophysics, Max-Planck-Institut fur Biophsikalische Chemie, Gottingen, Germany
The research focus of this laboratory is to understand the molecular and cellular mechanisms underlying chronic pain and nociception. We have concentrated our studies on plastic changes in cell signaling following inflammation and nerve injury. Dorsal root ganglion (DRG) neurons and dorsal horn neurons in the spinal cord and in the caudal medulla play a central role in the transmission and integration of nociceptive information. Understanding the receptor channel properties of these neurons, their responses to ATP, glutamate and opioids and the involvement of G-proteins and second messenger signaling under normal and injurious conditions has led to insights into the basis of abnormal sensory information processing in injurious states.
Another research focus is to understand the mechanism of ATP release between the cell body of a DRG neuron and its surrounding satellite glial cells and to determine the significance of this release, the involvement of purinergic receptors in neuron-satellite glial cell communication and changes in the communication after tissue and nerve injuries.
The third interest is to determine the applicability of our knowledge of pain processing obtained in rodents to humans. Attempts to use our understanding of opioid analgesia, obtained mainly from studies of rat models, in clinical trials often failed. To address this inadequacy, we determined opioid analgesia in sheep and found that the human equivalent ceiling dose calculated from sheep is much closer to the human morphine ceiling dose than that obtained from rats. This observation emphasizes the importance of using large animal models to validate the data obtained from rodent experiments before clinical trials.
Chen, L. and Huang L.-Y. M. Protein Kinase C reduces Mg2+ block of NMDA-receptor channels as a mechanism of modulation. Nature 356:521-523, 1992.
Huang L.-Y. M. and Neher, E. Ca2+-dependent exocytosis in the somata of dorsal root ganglion neurons. Neuron 17:135-145, 1996.
Xu G.-Y. and Huang L.-Y. M. Peripheral inflammation sensitizes P2X receptor mediated responses in rat dorsal root ganglion neurons. J. Neurosci. 22:93-102, 2002.
Xu, Y., Gu, Y., Xu, G.Y., Wu, P., Li, G.W., and Huang L.-Y.M. Adeno-associated viral transfer of opioid receptor gene to primary sensory neurons: A strategy to increase opioid antinociception. Proc. Natl. Acad. Sci.100:6204-6209, 2003.
Chen, Y., Gu, Y., Wang, C., Li, G.W. and Huang, L.-Y. M. Sensitization and enhanced trafficking of P2X3 receptors in the neuropathic pain state. Pain 119 38-48, 2005.
Wang, C., Gu, Y. Li, G.W., and Huang, L.-Y. M., A critical role of cAMP sensor Epac in switching protein kinase signaling in prostaglandin E2-induced potentiation of P2X3 receptor currents in inflamed rats J. Physiol (London) 584.1:191-203, 2007.
Zhang, X., Chen, Y, Wang, C. and Huang, L.-Y. M. Neuronal somatic ATP release triggers neuron-satellite glial cell communication in dorsal root ganglia, Proc. Natl. Acad. Sci. 104:9864-9869, 2007.
Chen, Y., Zhang, X., Wang, C. Li, G.W., Gu. Y. and Huang, L.-Y. M. Activation of P2X7 receptors in glial satellite cells reduces pain through downregulation of P2X3 receptors in nociceptive neurons, Proc. Natl. Acad. Sci. 105:16773-16778, 2008.
Wilkes, D., Li, G., Angeles, C. F., Patterson, J. T. and Huang, L.-Y. M. A large animal neuropathic pain model in sheep: a strategy for improving the predictability of preclinical models for therapeutic development. J. of Pain Research 5:415-424, 2012.
Gu, Y., Li G., Chen, Y. and Huang, L.-Y. M. Epac-PKCalpha signaling in purinergic P2X3R-mediated hyperalgesia after inflammation. Pain (In press).
Link to PubMed Publications