Claire Hulsebosch, Ph.D.

Dr. Hulsebosch received her B.A. in biology from Rice University in 1974, where she was a Jesse H. Jones and Mary Gibbs Jones Scholar. While at Rice, she was chairperson of the Student Academic Committee and actively involved in course development in the undergraduate curriculum. She pursued her interests in central nervous system regeneration as a doctoral dissertation project at The University of Texas at Austin, where she received her Ph.D. in neurosciences from the Department of Zoology in 1979. Concurrent with her graduate research, she worked as an electron microscopist for the Cell Research Institute in Austin. While a graduate student, she obtained a Kappa Gamma Fellowship and National Paralyzed Veterans Scholarship, and was nominated and accepted to Phi Kappa Phi. Awarded a three-year NIH postdoctoral fellowship, she came to the Marine Biomedical Institute in June 1979 to join the spinal cord research group. She was promoted to Assistant Professor in 1982, promoted with tenure to Associate Professor in 1989 and promoted to Full Professor in 1994. She currently has funds from NIH, the Spinal Cord Research Foundation, the Kent Waldrep Foundation, the RGK Foundation, and Mission Connect sponsored by The Institute of Rehabilitation and Research. An active course director of two courses in Cell Biology and the Neuroscience Graduate programs, she is committed to graduate education as evidenced by the success of the numerous doctoral dissertation students that she has supervised. She is actively involved in medical education as a professor in Human Gross Anatomy. For example, three of the studies of her students are currently in clinical phase I trials. These contributions to the teaching mission ensure that future generations will be prepared to challenge existing dogma.

Her current research efforts are focused on both acute and chronic interventions for the recovery of function after SCI with over 200 peer-reviewed articles and abstracts in this area. In addition, she has several publications and expertise in brain trauma and stroke. Her lab is supported by funds from NIH, including a Program Project Grant in Spinal Cord Injury, the Christopher Reeves Paralysis Foundation, the Spinal Cord Research Foundation, the Kent Waldrep Foundation, the RGK Foundation, the Dunn Foundation and Mission Connect sponsored by The Institute of Rehabilitation and Research and most recently was named Scientific Director of Mission Connect. Currently, she is Project Director of the UTMB Spinal Cord Injury Consortium, a group that was recently awarded a prestigious NIH Program Project Grant. She currently serves on the Scientific Advisory Board of several Spinal Cord Injury Foundations and journals, has served as Chair for several study sections and site visits for the National Institute for Neurological Disorders and Stroke, and has held offices in several national organizations, most recently President of the National Neurotrauma Society.

Research Interests

Our research interests are focused on central and peripheral nervous system regeneration mechanisms, as well as molecular aspects of the development and plasticity of these systems. With neuroanatomical techniques, including newer molecular approaches, it is possible to investigate the response of the nervous system after various manipulations as well as the molecular mechanisms involved in the response. For example, the mammalian spinal cord was once generally thought to be like a hard-wired circuit from birth. That is, once specific nerve connections were formed during development, these connections remained unchanged throughout the life of the organism. Contrary to this notion, neuroanatomical investigations during the past 30 years have suggested that the mammalian spinal cord remains plastic, or changeable, after birth and that central nervous system neurons sprout after injury. These studies are equivocal, however, since the anatomical techniques on which they are based cannot resolve the majority of axons that make up the mammalian nervous system. With the advent of the electron microscope, both coarse and fine fibers could be viewed and hence could be studied after various spinal cord injuries.

One important finding of the current research is that the fine-fiber population sprouts in response to denervation of the spinal cord. Other parameters of the sprouting response currently under investigation are the time course of the sprouting response; the synaptic connections of the sprouting population; the response of the sprouting population to various therapeutic factors, including nerve growth factor; and antibodies to nerve growth factor; and the molecular mechanisms that provide the basis for the sprouting response. We hope that when the parameters of sprouting are understood, behavioral deficits after spinal injury can be correlated and eventually ameliorated. Other objectives of this research are the following: 1) to investigate the development and plasticity of central and peripheral nervous system, 2) to investigate the responses of the central and peripheral nervous systems to various growth factors, and 3) to understand basic molecular principles that provide the proper microenvironment for neural sprouting.

We are investigating the mechanisms of recovery after spinal cord injury (SCI) using techniques which included molecular and pharmacological approaches to determine the basis for recovery of motor function and the development of chronic pain. In parallel experiments, we are characterizing cultured human fetal spinal neurons toward transplant therapy to replace injured neurons in SCI. A tangent of this work with respect to functional neuronal growth, has been the investigation of dysfunctional neuronal growth and the clinical diseases which result. Specifically, we are focusing currently on the underlying mechanisms of chronic central pain. Finally, in two models of brain injury, a focal cortical ischemia model (stroke) and a fluid percussion injury model (head trauma), we are investigating the expression of neurotrophins and exogenous application of neurotrophins, by injections, infusions or by cells transfected with neurotrophin genes, to rescue neurons which would otherwise die due to trauma. As an important outcome measure, reliable behavioral tests of each neurotrauma model have been developed and are used to assess the success of interventions toward improved recovery of function following central nervous system trauma.

Recent Publications

Hains, B.C., Johnson, K.M., Eaton, M.J., Willis, W.D. and Hulsebosch, C.E. Serotonergic neural precursor cell grafts attenuate bilateral hyperexcitability of dorsal horn neurons after spinal hemisection in rat. Neuroscience 116: 1097-1110, 2003.
Gwak, Y.S., Nam, T.S., Paik, K.S., Hulsebosch, C.E. and Leem, J.W. Attenuation of mechanical hyperalgesia following spinal cord injury by administration of antibodies to nerve growth factor in the rat. Neurosci. Lett. 336: 117-120, 2003.

Ondarza, A.B., Ye, Z. and Hulsebosch, C.E. Direct evidence of primary afferent sprouting in distant segments following spinal cord injury in the rat: colocalization of GAP-43 and CGRP. Exp. Neurol. 184: 373-380, 2003.

Xu, G-Y., Hughes, M.G., Ye, Z., Hulsebosch, C.E. and McAdoo, D.J. Concentrations of glutamate released following spinal cord injury kill oligodendrocytes in the spinal cord. Exp. Neurol. 187: 329-336, 2004.

Gwak, Y.S. and Hulsebosch, C.E. Effect of age at time of spinal cord injury on behavioral outcomes in rat. J. Neurotrauma 21:983-994, 2004.

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., Westlund, K.N., Hulsebosch, C.E. and Perez-Polo, J.R. Exogenous BCL-X(L) fusion spares neurons after spinal cord injury. J. Neurosci. Res. 79: 628-637, 2005.

McAdoo, D.J., Hughes, M.G., Nie, L., Shah, B., Clifton, C., Fullwood, S. and Hulsebosch, C.E. The effect of glutamate receptor blockers on glutamate release following spinal cord injury. Lack of evidence for an ongoing feedback cascade of damage -> glutamate release -> damage -> glutamate release -> etc. 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. (12) 384:139-44, 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 injuty. 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 on 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.., in press.



Claire Hulsebosch, Ph.D. cehulseb@utmb.edu Dr. Hulsebosch received her B.A. in biology from Rice University in 1974, where she was a Jesse H. Jones and Mary Gibbs Jones Scholar. While at Rice, she was chairperson of the Student Academic Committee and actively involved in course development in the undergraduate curriculum. She pursued her interests in central nervous system regeneration as a doctoral dissertation project at The University of Texas at Austin, where she received her Ph.D. in neurosciences from the Department of Zoology in 1979. Concurrent with her graduate research, she worked as an electron microscopist for the Cell Research Institute in Austin. While a graduate student, she obtained a Kappa Gamma Fellowship and National Paralyzed Veterans Scholarship, and was nominated and accepted to Phi Kappa Phi. Awarded a three-year NIH postdoctoral fellowship, she came to the Marine Biomedical Institute in June 1979 to join the spinal cord research group. She was promoted to Assistant Professor in 1982, promoted with tenure to Associate Professor in 1989 and promoted to Full Professor in 1994. She currently has funds from NIH, the Spinal Cord Research Foundation, the Kent Waldrep Foundation, the RGK Foundation, and Mission Connect sponsored by The Institute of Rehabilitation and Research. An active course director of two courses in Cell Biology and the Neuroscience Graduate programs, she is committed to graduate education as evidenced by the success of the numerous doctoral dissertation students that she has supervised. She is actively involved in medical education as a professor in Human Gross Anatomy. For example, three of the studies of her students are currently in clinical phase I trials. These contributions to the teaching mission ensure that future generations will be prepared to challenge existing dogma. Her current research efforts are focused on both acute and chronic interventions for the recovery of function after SCI with over 200 peer-reviewed articles and abstracts in this area. In addition, she has several publications and expertise in brain trauma and stroke. Her lab is supported by funds from NIH, including a Program Project Grant in Spinal Cord Injury, the Christopher Reeves Paralysis Foundation, the Spinal Cord Research Foundation, the Kent Waldrep Foundation, the RGK Foundation, the Dunn Foundation and Mission Connect sponsored by The Institute of Rehabilitation and Research and most recently was named Scientific Director of Mission Connect. Currently, she is Project Director of the UTMB Spinal Cord Injury Consortium, a group that was recently awarded a prestigious NIH Program Project Grant. She currently serves on the Scientific Advisory Board of several Spinal Cord Injury Foundations and journals, has served as Chair for several study sections and site visits for the National Institute for Neurological Disorders and Stroke, and has held offices in several national organizations, most recently President of the National Neurotrauma Society. Research Interests Our research interests are focused on central and peripheral nervous system regeneration mechanisms, as well as molecular aspects of the development and plasticity of these systems. With neuroanatomical techniques, including newer molecular approaches, it is possible to investigate the response of the nervous system after various manipulations as well as the molecular mechanisms involved in the response. For example, the mammalian spinal cord was once generally thought to be like a hard-wired circuit from birth. That is, once specific nerve connections were formed during development, these connections remained unchanged throughout the life of the organism. Contrary to this notion, neuroanatomical investigations during the past 30 years have suggested that the mammalian spinal cord remains plastic, or changeable, after birth and that central nervous system neurons sprout after injury. These studies are equivocal, however, since the anatomical techniques on which they are based cannot resolve the majority of axons that make up the mammalian nervous system. With the advent of the electron microscope, both coarse and fine fibers could be viewed and hence could be studied after various spinal cord injuries. One important finding of the current research is that the fine-fiber population sprouts in response to denervation of the spinal cord. Other parameters of the sprouting response currently under investigation are the time course of the sprouting response; the synaptic connections of the sprouting population; the response of the sprouting population to various therapeutic factors, including nerve growth factor; and antibodies to nerve growth factor; and the molecular mechanisms that provide the basis for the sprouting response. We hope that when the parameters of sprouting are understood, behavioral deficits after spinal injury can be correlated and eventually ameliorated. Other objectives of this research are the following: 1) to investigate the development and plasticity of central and peripheral nervous system, 2) to investigate the responses of the central and peripheral nervous systems to various growth factors, and 3) to understand basic molecular principles that provide the proper microenvironment for neural sprouting. We are investigating the mechanisms of recovery after spinal cord injury (SCI) using techniques which included molecular and pharmacological approaches to determine the basis for recovery of motor function and the development of chronic pain. In parallel experiments, we are characterizing cultured human fetal spinal neurons toward transplant therapy to replace injured neurons in SCI. A tangent of this work with respect to functional neuronal growth, has been the investigation of dysfunctional neuronal growth and the clinical diseases which result. Specifically, we are focusing currently on the underlying mechanisms of chronic central pain. Finally, in two models of brain injury, a focal cortical ischemia model (stroke) and a fluid percussion injury model (head trauma), we are investigating the expression of neurotrophins and exogenous application of neurotrophins, by injections, infusions or by cells transfected with neurotrophin genes, to rescue neurons which would otherwise die due to trauma. As an important outcome measure, reliable behavioral tests of each neurotrauma model have been developed and are used to assess the success of interventions toward improved recovery of function following central nervous system trauma. Recent Publications Hains, B.C., Johnson, K.M., Eaton, M.J., Willis, W.D. and Hulsebosch, C.E. Serotonergic neural precursor cell grafts attenuate bilateral hyperexcitability of dorsal horn neurons after spinal hemisection in rat. Neuroscience 116: 1097-1110, 2003. Gwak, Y.S., Nam, T.S., Paik, K.S., Hulsebosch, C.E. and Leem, J.W. Attenuation of mechanical hyperalgesia following spinal cord injury by administration of antibodies to nerve growth factor in the rat. Neurosci. Lett. 336: 117-120, 2003. Ondarza, A.B., Ye, Z. and Hulsebosch, C.E. Direct evidence of primary afferent sprouting in distant segments following spinal cord injury in the rat: colocalization of GAP-43 and CGRP. Exp. Neurol. 184: 373-380, 2003. Xu, G-Y., Hughes, M.G., Ye, Z., Hulsebosch, C.E. and McAdoo, D.J. Concentrations of glutamate released following spinal cord injury kill oligodendrocytes in the spinal cord. Exp. Neurol. 187: 329-336, 2004. Gwak, Y.S. and Hulsebosch, C.E. Effect of age at time of spinal cord injury on behavioral outcomes in rat. J. Neurotrauma 21:983-994, 2004. 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., Westlund, K.N., Hulsebosch, C.E. and Perez-Polo, J.R. Exogenous BCL-X(L) fusion spares neurons after spinal cord injury. J. Neurosci. Res. 79: 628-637, 2005. McAdoo, D.J., Hughes, M.G., Nie, L., Shah, B., Clifton, C., Fullwood, S. and Hulsebosch, C.E. The effect of glutamate receptor blockers on glutamate release following spinal cord injury. Lack of evidence for an ongoing feedback cascade of damage -> glutamate release -> damage -> glutamate release -> etc. 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. (12) 384:139-44, 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 injuty. 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 on 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.., in press.
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