Claire E. Hulsebosch, Ph.D.
Vice-Chair and Professor
Claire E. Hulsebosch, Ph.D.
B.A. (Biology), Rice University, Houston, Texas
• Ph.D. (Zoology), University of Texas, Austin, Texas
About the Lab
Spinal cord injury results in a variety of changes that continue to be cytotoxic to cells that are at risk of dying, both nerve cells and glial cells-cells that are not nerve cells but are critical for normal spinal cord function. Her group reports that nerve cells and glial cells are changed permanently after spinal cord injury. They are in the process of using molecular, behavioral, physiological, immunocytochemical and electrophysiological approaches to study the mechanisms that underlie the permanent changes that will help restore the spinal cord to normal function. Her collaborative manuscripts demonstrate numerous publications that described permanent changes that are many segments above and below the spinal cord injury and persistent changes in neural circuits in these regions that lead to dysfunction. One project is focused on recovery of normal sensory/motor function; another project focuses on improved visceral function, while other projects test the role of transplanted cells. For example, her laboratory has demonstrated that molecularly engineered cells transplanted onto the surface of the spinal cord can return the abnormal characteristics of the nerve cells that develop after SCI, to more normal behavior. They hypothesize that persistent neuroinflammation in the spinal cord contributes to permanent alterations in nerve cell circuits, and that the abnormal reaction of microglia and astrocytes after SCI (she calls this “gliopathy”), even many segments away continues to contribute to the neuroinflammation leading to impaired nerve cell function. Insight in these pathways will suggest therapeutic intervention strategies.
Currently, Dr. Hulsebosch is part of the scientific advisory board for both the Neurological Recovery Network and the North American Clinical Trials Network, which are actively involved in advancing clinical trials in spinal cord injury. She serves as scientific advisor to the National Institute of Health for Neuroscience Initiatives, on study section for National Institute of Neurological Diseases and Stroke, on the Christopher and Dana Reeves Foundation, the New Jersey Commission for Spinal Cord Injury Research, The Kentucky Initiative for Brain and Spinal Cord Injury Research, The New York Commission for Spinal Cord injury Research and a variety of editorial and review boards for scientific journals. She served as Director of Mission Connect from 2005 to 2008 and was the lead for UTMB’s involvement during the formative years of Mission Connect, which is now experiencing its 11th year of research advances.
How Dr. Hulsebosch’s research relates to Mission Connect
Mission Connect is a multi-institutional research group whose mission is to advance research for recovery after brain and spinal cord injury. This is consistent with the more than 300 publications and presentations from her laboratory. She pioneered the concept of nerve cell process reorganization and the formation of new nerve connections (synatogenesis) in the spinal cord after injury. She has numerous publications that demonstrate the ability of nerve cells to reorganize after spinal cord injury. In addition, she has several publications examining the ability of nerve fibers to reorganize after brain injury and stroke. Three of the interventions described by her laboratory are in clinical trials, or are in use as an off label clinical strategy to improve function after spinal cord injury. The new discovery of chronic neuroinflammation process provides a mechanism for continued research to improve function after spinal cord injury. She served as Mission Connect Director from 2005 to 2008 during which time the Moody Center for Brain and Spinal Cord Injury Research/Mission Connect was established at University Of Texas Medical Branch Galveston; University Of Texas Health Science Center/Mission Connect began its development; Baylor recruited three nationally renowned neuroscientists that joined Mission Connect, Project Victory for aggressive rehabilitation and community reintegration for our injured troops returning from the Middle East and the award of the Mission Connect Department of Defense 33M award in Mild Traumatic Brain Injury.
Research – Lay Description
There are several research programs currently ongoing in our group that focus on acute and chronic intervention for spinal cord injury (SCI) treatment. SCI occurs most frequently to young (16 to 25 yrs) individuals and severely alters not only locomotion but also the sensory experience, which includes abnormal chronic pain syndromes that develops months to years after injury. She uses techniques that span live animal behavior, surgery, protein chemistry, immunocytochemistry, gene interventions, transplantation of engineered cells, to list a few. Her laboratory moves research from the bench top and brings it to the threshold of clinical trials. She is currently active in several clinical trials as a scientific advisory. Her laboratory truly extends from molecules to man in its research approach.
Hulsebosch, C.E. Mechanisms and treatment strategies for chronic central neuropathic pain after spinal cord injury. Top. Spinal Cord Inj. Rehabil. 8: 76-91, 2003.
Hulsebosch, C.E. Central sensitization and pain after spinal cord injury. Sem. Pain Med. 1: 159-170, 2003.
McAdoo,D.J.,Hughes,M.G., Nie,L. Shah,B., Cannon,D., Fullwood,S.,Hulsebosch,C.E. The effect of gulatamate receptor blockers on glutamate release following spinal cord injury. Brain Res.1038: 92-99, 2005.
Hulsebosch, C.E. From discovery to clinical trials: Treatment strategies for central neuropathic pain after spinal cord injury. Current Pharmaceutical Design 11: 1411-1420, 2005.
Crown, E.D., Ye, Z., Johnson, K.M., Xu, G-Y., McAdoo, D.J., Westlund, K.N. and Hulsebosch, C.E. Upregulation of the phosphorylated form of CREB in spinothalamic tract cells following spinal cord injury: Relation to central neuropathic pain. Neurosci. Lett. 384: 139-144, 2005.
Gwak, Y.S. and Hulsebosch, C.E. Upregulation of Group I metabotropic glutamate receptors in neurons and astrocytes in the dorsal horn following spinal cord injury. Exp. Neurol. 195: 236-243, 2005.
Dussor, G.O., Jones, D.J., Hulsebosch, C.E., Edell, T.A. and Flores, C.M. The effects of chemical or surgical deafferentation on [3H]-acetylcholine release from rat spinal cord. Neuroscience 135: 1269-1276, 2005.
Nesic, O., Lee, J., Johnson, K.M., Ye, Z., Xu, G-Y., Unabia, G.C., Wood, T.G., McAdoo, D.J., Westlund, K.N., Hulsebosch, C.E. and Perez-Polo, J.R. Transcriptional profiling of spinal cord injury-induced central neuropathic pain. J. Neurochem. 95: 998-1014, 2005.
Nesic-Taylor, O., Cittelly, D., Ye, Z., Xu, G-Y., Unabia, G., Lee, J.C., Svrakic, N.M., Liu, X-H., Youle, R.J., Wood, T.G., McAdoo, D.J., Westlund, K.N., Hulsebosch, C.E. and Perez-Polo, J.R. Exogenous Bcl-xL fusion protein spares neurons after spinal cord injury. J. Neurosci. Res. 79: 628-637, 2005.
Crown, E.D., Ye, Z., Johnson, K.M., Xu, G-Y., McAdoo, D.J. and Hulsebosch, C.E. Increases in the activated forms of ERK ½, p38 MAPK, and CREB are correlated with the expression of at-level mechanical allodynia following spinal cord injury. Exp. Neurol. 199: 397-407, 2006.
Gwak, Y.S., Tan, H., Nam, T.S., Paik, K.S., Hulsebosch, C.E. and Leem, J.W. Activation of spinal GABA receptors attenuates chronic central neuropathic pain after spinal cord injury. J. Neurotrauma 23: 1111-1124, 2006.
Tarasenko, Y.I., Gao, J., Nie, L., Johnson, K.M., Grady, J.J., Hulsebosch, C.E., McAdoo, D.J. and Wu, P. Human fetal stem cells grafted into contusion-injured rat spinal cord improve behavior. J. Neurosci. Res. 85: 47-57, 2007.
Nesic, O., Lee, J., Ye, Z., Unabia, G.C., Rafati, D., Hulsebosch, C.E. and Perez-Polo, J.R. Acute and chronic changes in aquaporin 4 expression after spinal cord injury. Neuroscience 143: 779-792, 2006.
Rooney, B.A., Crown, E.D. and Hulsebosch, C.E. Preemptive analgesia with lidocaine prevents failed back surgery syndrome. Exp. Neurol. 204: 589-596, 2007.
Gwak, Y.S., Kang, J., Leem, J.W. and Hulsebosch, C.E. Spinal AMPA receptor inhibition attenuates mechanical allodynia and neuronal hyperexcitability following spinal cord injury in rats. J. Neurosci. Res. 85: 2352-2359, 2007
Acute, subacute and chronic models of spinal cord injury
traumatic brain injury
regeneration and repair