The role of ionotropic glutamate receptors in chronic central pain after spinal cord injury

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The role of ionotropic glutamate receptors in chronic central pain after spinal cord injury

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dc.contributor.advisor Claire Hulsebosch, Ph.D. en_US
dc.creator Huaiyu Tan en_US
dc.date.accessioned 2011-12-20T16:05:45Z
dc.date.available 2009-06-09 en_US
dc.date.available 2011-12-20T16:05:45Z
dc.date.created 2005-12-21 en_US
dc.date.issued 2005-12-12 en_US
dc.identifier.other etd-12212005-164154 en_US
dc.identifier.uri http://hdl.handle.net/2152.3/298
dc.description.abstract Spinal cord injury (SCI) results in both loss of function and chronic central pain syndromes. In the clinical population, pain is characterized based on anatomical location: 1) Below-level pain – located at dermatomes corresponding to spinal segments caudal to the injury site, 2) At-level pain – located at dermatomes corresponding to spinal segments immediately adjacent to the injury site, 3) Above-level pain – located at segments rostral to the injury site (in area of sensory preservation). \r\n A contusion model of SCI was first characterized behaviorally and electrophysiologically. A contusion at spinal segment T10 at 150 kdynes of force and a 1 second dwell time resulted in the pain like behavior in the hindlimbs, thoracic region, and forelimbs 35 days post-injury. These contused animals exhibited spinal hyperexcitability during extracellular single-unit electrophysiological spinal recordings from the dorsal horn of the lumbar enlargement (below-level), thoracic cord (at-level; immediately rostral to injury site), and brachial enlargement (above level). \r\n In models of peripheral injury, increased ionotropic glutamate receptor mediated activity results in spinal central sensitization. Extracellular single-unit recordings from all three regions of the spinal cord (lumbar enlargement, thoracic cord, and brachial enlargement) were made on both contused and non-contused animals during ionotropic glutamate antagonist treatment (D-AP5 or NBQX). The thoracic cord, which is nearest to the site of injury, showed the greatest increase in ionotropic glutamate receptor mediated activity. \r\n Calcium-calmodulin protein kinase II (CaMKII) has been shown to be responsible for enhancing ionotropic glutamate receptor mediated activity. CaMKII also has been shown to be a molecular intermediate in both long-term potentiation (LTP) and peripherally induced central sensitization. After contusive SCI, the segments immediately rostral to the injury site show an increase in activated CaMKII. Application of CaMKII inhibitor, KN-93, during recording 35 days post injury, reduces spinal hyperexcitability induced by SCI. \r\n en_US
dc.format.medium electronic en_US
dc.language.iso eng en_US
dc.rights Copyright © is held by the author. Presentation of this material on the TDL web site by The University of Texas Medical Branch at Galveston was made possible under a limited license grant from the author who has retained all copyrights in the works. en_US
dc.subject NBQX en_US
dc.subject KN-93 en_US
dc.subject D-AP5 en_US
dc.title The role of ionotropic glutamate receptors in chronic central pain after spinal cord injury en_US
dc.type.material text en_US
dc.type.genre dissertation en_US
thesis.degree.name PhD en_US
thesis.degree.level Doctoral en_US
thesis.degree.grantor The University of Texas Medical Branch en_US
thesis.degree.department Neuroscience and Cell Biology en_US
dc.contributor.committeeMember William D. Willis, M.D./Ph.D. en_US
dc.contributor.committeeMember Volker E. Neugebauer, M.D./Ph.D. en_US
dc.contributor.committeeMember Martin Grabois, M.D. en_US
dc.contributor.committeeMember B. Mark Evers, M.D. en_US

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