{"id":{"repo_id":"utmb","oai_identifier":"oai:utmb-ir.tdl.org:2152.3/260"},"canonical_url":"https://search.dev.ndltd.org/etd/utmb/oai:utmb-ir.tdl.org:2152.3/260","repository":{"repo_id":"utmb","name":"University of Texas Medical Branch","base_url":"https://utmb-ir.tdl.org/server/oai/request"},"display":{"title":"Roles of interleukin-1 beta in glutamate-induced spinal cord injury","abstract":"Glutamate release contributes to the impairments caused by spinal cord injury (SCI). This study addresses the mechanisms of glutamate toxicity involving activation of interleukin-1â (IL-1â). To assess the effects of glutamate on IL-1â and its natural blocking agent interleukin-1 receptor antagonist (IL-1ra), ELISA assays were used to measure the responses of endogenous IL-1â and IL-1ra to glutamate administered to the spinal cord. Levels of activated IL-1â and IL-1ra changed in a reciprocal fashion starting 1 hour after glutamate exposure. Exposure to glutamate initially increases IL-1â expression while it decreases IL-1ra. IL-1â then decreases and IL-1ra increases. IL-1â and IL-1ra change reciprocally in the same fashion in a contused spinal cord. To check whether this mutual effect is due to actions of IL-1â and IL-1ra on each other, IL-1â was applied on the spinal cord and then IL-1ra was measured. IL-1ra was applied onto the cord and IL-1â was measured as well. The results show that administration of IL-1â stimulates the production of IL-1ra and administration of IL-1ra suppresses the activation of IL-1â. To identify subtypes of glutamate receptors involved in this phenomenon, NMDA and AMPA receptor agonists were separately applied to the spinal cord and IL-1â and IL-1ra expression in the cord were measured with ELISA assays. Activation of both the AMPA and the NMDA receptors also induced reciprocal changes between the IL-1â and IL-1ra levels. To determine the effects of activating AMPA and NMDA receptors on IL-1â and IL-1ra, MK801 and NBQX were applied individually on the spinal cord with glutamate. The results show that both AMPA and NMDA receptors are involved in glutamate-induced reciprocity between IL-1â and IL-1ra. To determine if this reciprocity between the expression of IL-1â and IL-1ra affected post-SCI locomotor function, recombinant IL-1â and IL-1ra were administered to glutamate-exposed spinal cords. The Basso-Beattie-Bresnahan (BBB) test of functional recovery demonstrated that IL-1â impaired rat locomotive ability and that IL-1ra improved the recovery of the rats from glutamate-induced locomotor impairment. To explore the mechanism of this IL-1â involvement in excitotoxicity, MAPK activities responding to glutamate were measured and the results showed that both ERK1/2 and p38 are involved in IL-1â induced SCI. Cell death assays showed that apoptosis is caused by glutamate-induced SCI. Overall, we established the following pathway from spinal cord injury to functional impairment: SCI → glutamate release → IL-1â and IL-1ra changes → ERK1/2 and p38 activation → cell death → functional impairment. This is the first pathway traced from glutamate release to functional impairments.","abstract_html":"Glutamate release contributes to the impairments caused by spinal cord injury (SCI). This study addresses the mechanisms of glutamate toxicity involving activation of interleukin-1â (IL-1â). To assess the effects of glutamate on IL-1â and its natural blocking agent interleukin-1 receptor antagonist (IL-1ra), ELISA assays were used to measure the responses of endogenous IL-1â and IL-1ra to glutamate administered to the spinal cord. Levels of activated IL-1â and IL-1ra changed in a reciprocal fashion starting 1 hour after glutamate exposure. Exposure to glutamate initially increases IL-1â expression while it decreases IL-1ra. IL-1â then decreases and IL-1ra increases. IL-1â and IL-1ra change reciprocally in the same fashion in a contused spinal cord. To check whether this mutual effect is due to actions of IL-1â and IL-1ra on each other, IL-1â was applied on the spinal cord and then IL-1ra was measured. IL-1ra was applied onto the cord and IL-1â was measured as well. The results show that administration of IL-1â stimulates the production of IL-1ra and administration of IL-1ra suppresses the activation of IL-1â. To identify subtypes of glutamate receptors involved in this phenomenon, NMDA and AMPA receptor agonists were separately applied to the spinal cord and IL-1â and IL-1ra expression in the cord were measured with ELISA assays. Activation of both the AMPA and the NMDA receptors also induced reciprocal changes between the IL-1â and IL-1ra levels. To determine the effects of activating AMPA and NMDA receptors on IL-1â and IL-1ra, MK801 and NBQX were applied individually on the spinal cord with glutamate. The results show that both AMPA and NMDA receptors are involved in glutamate-induced reciprocity between IL-1â and IL-1ra. To determine if this reciprocity between the expression of IL-1â and IL-1ra affected post-SCI locomotor function, recombinant IL-1â and IL-1ra were administered to glutamate-exposed spinal cords. The Basso-Beattie-Bresnahan (BBB) test of functional recovery demonstrated that IL-1â impaired rat locomotive ability and that IL-1ra improved the recovery of the rats from glutamate-induced locomotor impairment. To explore the mechanism of this IL-1â involvement in excitotoxicity, MAPK activities responding to glutamate were measured and the results showed that both ERK1/2 and p38 are involved in IL-1â induced SCI. Cell death assays showed that apoptosis is caused by glutamate-induced SCI. Overall, we established the following pathway from spinal cord injury to functional impairment: SCI → glutamate release → IL-1â and IL-1ra changes → ERK1/2 and p38 activation → cell death → functional impairment. This is the first pathway traced from glutamate release to functional impairments.","abstract_has_math":false,"creators":["Song Liu"],"institution":"The University of Texas Medical Branch","degree_name":"PhD","degree_level":"Doctoral","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["David McAdoo"],"committee_chairs":[],"committee_members":["Raymond Grill","Ping Wu","Allan Brasier","Alex Kurosky"],"year":2006,"date_issued":"2006-11-15","date_published":"2006-11-15","updated_at":"2026-07-24T05:51:01Z","subjects":["spinal cord injury","MAPKs","IL-1ra","IL-1â","glutamate"],"languages":["eng"],"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."],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-11172006-151805"],"render_values":[{"text":"etd-11172006-151805","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2152.3/260","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["David McAdoo"]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Raymond Grill","Ping Wu","Allan Brasier","Alex Kurosky"]},{"key":"dc:creator","label":"Author","values":["Song Liu"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2011-12-20T16:05:33Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2009-06-09","2011-12-20T16:05:33Z"]},{"key":"dc:date.issued","label":"Date","values":["2006-11-15"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["PhD"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["The University of Texas Medical Branch"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["spinal cord injury","MAPKs","IL-1ra","IL-1â","glutamate"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["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."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-11172006-151805"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/2152.3/260"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Glutamate release contributes to the impairments caused by spinal cord injury (SCI). This study addresses the mechanisms of glutamate toxicity involving activation of interleukin-1â (IL-1â). To assess the effects of glutamate on IL-1â and its natural blocking agent interleukin-1 receptor antagonist (IL-1ra), ELISA assays were used to measure the responses of endogenous IL-1â and IL-1ra to glutamate administered to the spinal cord. Levels of activated IL-1â and IL-1ra changed in a reciprocal fashion starting 1 hour after glutamate exposure. Exposure to glutamate initially increases IL-1â expression while it decreases IL-1ra. IL-1â then decreases and IL-1ra increases. IL-1â and IL-1ra change reciprocally in the same fashion in a contused spinal cord. To check whether this mutual effect is due to actions of IL-1â and IL-1ra on each other, IL-1â was applied on the spinal cord and then IL-1ra was measured. IL-1ra was applied onto the cord and IL-1â was measured as well. The results show that administration of IL-1â stimulates the production of IL-1ra and administration of IL-1ra suppresses the activation of IL-1â. To identify subtypes of glutamate receptors involved in this phenomenon, NMDA and AMPA receptor agonists were separately applied to the spinal cord and IL-1â and IL-1ra expression in the cord were measured with ELISA assays. Activation of both the AMPA and the NMDA receptors also induced reciprocal changes between the IL-1â and IL-1ra levels. To determine the effects of activating AMPA and NMDA receptors on IL-1â and IL-1ra, MK801 and NBQX were applied individually on the spinal cord with glutamate. The results show that both AMPA and NMDA receptors are involved in glutamate-induced reciprocity between IL-1â and IL-1ra. To determine if this reciprocity between the expression of IL-1â and IL-1ra affected post-SCI locomotor function, recombinant IL-1â and IL-1ra were administered to glutamate-exposed spinal cords. The Basso-Beattie-Bresnahan (BBB) test of functional recovery demonstrated that IL-1â impaired rat locomotive ability and that IL-1ra improved the recovery of the rats from glutamate-induced locomotor impairment. To explore the mechanism of this IL-1â involvement in excitotoxicity, MAPK activities responding to glutamate were measured and the results showed that both ERK1/2 and p38 are involved in IL-1â induced SCI. Cell death assays showed that apoptosis is caused by glutamate-induced SCI. Overall, we established the following pathway from spinal cord injury to functional impairment: SCI → glutamate release → IL-1â and IL-1ra changes → ERK1/2 and p38 activation → cell death → functional impairment. This is the first pathway traced from glutamate release to functional impairments."]},{"key":"dc:format.medium","label":"Dc Format Medium","values":["electronic"]},{"key":"dc:title","label":"Title","values":["Roles of interleukin-1 beta in glutamate-induced spinal cord injury"]}]}],"canonical_facts":{"dc:contributor.advisor":["David McAdoo"],"dc:contributor.committeemember":["Raymond Grill","Ping Wu","Allan Brasier","Alex Kurosky"],"dc:creator":["Song Liu"],"dc:date.accessioned":["2011-12-20T16:05:33Z"],"dc:date.available":["2009-06-09","2011-12-20T16:05:33Z"],"dc:date.issued":["2006-11-15"],"dc:description.abstract":["Glutamate release contributes to the impairments caused by spinal cord injury (SCI). This study addresses the mechanisms of glutamate toxicity involving activation of interleukin-1â (IL-1â). To assess the effects of glutamate on IL-1â and its natural blocking agent interleukin-1 receptor antagonist (IL-1ra), ELISA assays were used to measure the responses of endogenous IL-1â and IL-1ra to glutamate administered to the spinal cord. Levels of activated IL-1â and IL-1ra changed in a reciprocal fashion starting 1 hour after glutamate exposure. Exposure to glutamate initially increases IL-1â expression while it decreases IL-1ra. IL-1â then decreases and IL-1ra increases. IL-1â and IL-1ra change reciprocally in the same fashion in a contused spinal cord. To check whether this mutual effect is due to actions of IL-1â and IL-1ra on each other, IL-1â was applied on the spinal cord and then IL-1ra was measured. IL-1ra was applied onto the cord and IL-1â was measured as well. The results show that administration of IL-1â stimulates the production of IL-1ra and administration of IL-1ra suppresses the activation of IL-1â. To identify subtypes of glutamate receptors involved in this phenomenon, NMDA and AMPA receptor agonists were separately applied to the spinal cord and IL-1â and IL-1ra expression in the cord were measured with ELISA assays. Activation of both the AMPA and the NMDA receptors also induced reciprocal changes between the IL-1â and IL-1ra levels. To determine the effects of activating AMPA and NMDA receptors on IL-1â and IL-1ra, MK801 and NBQX were applied individually on the spinal cord with glutamate. The results show that both AMPA and NMDA receptors are involved in glutamate-induced reciprocity between IL-1â and IL-1ra. To determine if this reciprocity between the expression of IL-1â and IL-1ra affected post-SCI locomotor function, recombinant IL-1â and IL-1ra were administered to glutamate-exposed spinal cords. The Basso-Beattie-Bresnahan (BBB) test of functional recovery demonstrated that IL-1â impaired rat locomotive ability and that IL-1ra improved the recovery of the rats from glutamate-induced locomotor impairment. To explore the mechanism of this IL-1â involvement in excitotoxicity, MAPK activities responding to glutamate were measured and the results showed that both ERK1/2 and p38 are involved in IL-1â induced SCI. Cell death assays showed that apoptosis is caused by glutamate-induced SCI. Overall, we established the following pathway from spinal cord injury to functional impairment: SCI → glutamate release → IL-1â and IL-1ra changes → ERK1/2 and p38 activation → cell death → functional impairment. This is the first pathway traced from glutamate release to functional impairments."],"dc:format.medium":["electronic"],"dc:identifier.other":["etd-11172006-151805"],"dc:identifier.uri":["http://hdl.handle.net/2152.3/260"],"dc:language.iso":["eng"],"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."],"dc:subject":["spinal cord injury","MAPKs","IL-1ra","IL-1â","glutamate"],"dc:title":["Roles of interleukin-1 beta in glutamate-induced spinal cord injury"],"thesis:degree_level":["Doctoral"],"thesis:degree_name":["PhD"],"thesis:institution_name":["The University of Texas Medical Branch"]},"updated_at":"2026-07-24T05:51:01Z"}