Student Highlight: Bryan Hains

BIOGRAPHICAL INFORMATION:

Post-Doctoral Fellow, PVA-EPVA Center for Neuroscience and Regeneration Research, and Department of Neurology, Yale University School of Medicine, Laboratory of Dr. Stephen G. Waxman. 2001-current.

Associate member (Postdoctoral Fellow), Marine Biomedical Institute, University of Texas Medical Branch, 2001.

Ph.D. (Neuroscience), University of Texas Medical Branch, September 2001. Dissertation: “Engraftment of 5-HT/BDNF-secreting serotonergic precursors enhances locomotor recovery and attenuates chronic central pain following spinal hemisection injury.” Supervisory professor, Dr. Claire E. Hulsebosch.

M.A. (Neurobiology), Boston University, August 1996. Thesis ”The role of the vomeronasal organ/accessory olfactory system in synaptic plasticity and neuroendocrine regulation of reproductive behavior."

B.S. (Biology, Chemistry), Stetson University, May 1995. Senior research: "Ibotenic acid lesions in the central nucleus of the amygdala and substance P in the rostral nucleus of the solitary tract in rats."


SUMMARY OF RESEARCH:

PVA-EPVA Center for Neuroscience and Regeneration Research, and Department of Neurology, Yale University School of Medicine:
Somatosensory neurons utilize voltage-gated Na channels to relay information from the periphery to the brain about innocuous and noxious stimuli. After spinal cord injury, alterations in how these impulses are propagated by Na channels are thought to contribute to the development of abnormal pain syndromes (ie: non-painful stimuli become painful, pain thresholds are lowered, normal pain is exaggerated). My work will examine the molecular plasticity of various types of these Na channels (SNS/Nav1.8, NaN/Nav1.9) and how their deployment effects the electrical properties of sensory neurons after injury with the hope of finding new and effective treatment strategies.

University of Texas Medical Branch:
My dissertation work focused on understanding the pathophysiological mechanisms of spinal cord injury and developing a novel treatment strategies. More specifically, I examined the changes in serotonergic elements in a rodent model of SCI, effects of intrathecally-injected compounds on excitability of dorsal horn neurons, and abnormal pain behaviors (mechanical allodynia and thermal hyperalgesia) that develop after injury. An understanding of these phenomena led to the development of a cell-based therapy whereby neurons genetically engineered to secrete growth-promoting (trophic) and pain-reducing compounds (antinociceptive) were successful in significantly promoting recovery of locomotor function and attenuating chronic central pain syndromes.

PEER-REVIEWED PUBLICATIONS:

1. Hains BC, Chastain KM, Everhart A.W, McAdoo DJ, Hulsebosch CE. Transplants of adrenal medullary chromaffin cells reduce mechanical and thermal allodynia in a model of chronic central pain after spinal cord injury. Exp. Neurol. 164: 426-437, 2000.

2. Hulsebosch CE, Hains BC, Waldrep K., Young W. Bridging the gap: From discovery to clinical trails in spinal cord injury. J. Neurotrauma 17: 1117-1128, 2000.

3. Hains BC. Yucra JA, Hulsebosch CE. Selective COX-2 inhibition with NS-398 preserves spinal parenchyma and attenuates behavioral deficits following spinal contusion injury. J. Neurotrauma 18: 409-423, 2001.

4. Mills CD, Hains BC, Johnson KM, Hulsebosch CE. Strain and model dependence of locomotor deficits and development of chronic central pain after spinal cord injury. J. Neurotrauma 18: 743-756, 2001.

5. Hains BC, Fullwood SD, Eaton MJ, Hulsebosch CE. Subdural engraftment of serotonergic neurons following spinal hemisection restores spinal serotonin, downregulates serotonin transporter, and increases BDNF tissue content in rat. Brain Res. 913: 35-46, 2001.

6. Hains BC, Johnson KM, Eaton MJ, Hulsebosch CE. Engraftment of serotonergic precursors enhances locomotor function and attenuates chronic central pain behavior following spinal hemisection injury in the rat. Exp. Neurol. 171: 361-378, 2001.

7. Hains BC, Hulsebosch CE, Willis WD. Differential effects of BDNF on spinal dorsal horn neurons after spinal cord hemisection injury. Neurosci. Lett. accepted, December, 2001.

8. Hains BC, Everhart AW, Hulsebosch CE. Serotonin and serotonin transporter mediated behavioral deficits after spinal hemisection are modulated by intrathecal 5-HT, antagonists, and reuptake inhibitors. Exp. Neurol. in revision, October, 2001.

9. Hains BC, Willis WD, Hulsebosch CE. Spinal hemisection induces chronic central sensitization in spinal dorsal horn neurons that is modulated by 5-HT. J. Neurophys. in revision, October, 2001.

10.  Hains BC, Eaton MJ, Willis WD, Hulsebosch CE. Engraftment of serotonergic precursors amends hyperexcitability of dorsal horn neurons after spinal hemisection-induced central sensitization. J. Neurosci. in revision, October, 2001.

11. Hains BC, Yucra JA, Hulsebosch CE. Intra-lesion transplantation of serotonergic precursors enhances locomotor recovery but has no effect on development of chronic central pain following hemisection injury. Neurosci. Lett. submitted, November, 2001.

12. McAdoo DJ, Hains BC, Hulsebosch CE. Exogenous LIF treatment attenuates the development of allodynia after spinal cord injury. In preparation.

13.  McAdoo DJ, Hains BC, Hulsebosch CE. Expression of LIF after spinal cord injury. In preparation.