rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    non sort: The
    title: role of tumor necrosis factor-alpha in maladaptive spinal plasticity
  name:
    name part: Huie, John Russell.
    role:
      role term: creator
  name:
    name part: Grau, James W.
    role:
      role term: thesis advisor.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2012
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource.
  abstract: Previous work has shown that the spinal cord is capable of supporting a simple form of instrumental learning. Subjects that receive controllable shock to an extended hind limb will increase the duration of limb flexion over time in order to reduce net shock exposure. Exposure to as little as 6 minutes of uncontrollable stimulation prior to instrumental testing can elicit a long-lasting learning deficit. Prior work has suggested that this deficit may reflect an overexcitation of spinal neurons akin to central sensitization, and that learning is inhibited by the saturation of plasticity. The experiments in this dissertation were designed to test the role of the cytokine tumor necrosis factor alpha (TNF[alpha]) in the induction and expression of the deficit. It is believed that the inflammatory properties of TNF[alpha] may mediate the excitatory processes that lead to maladaptive spinal functioning. Experiments 1 and 2 tested the necessity of endogenous TNF[alpha] in the deficit produced by uncontrollable shock. These experiments showed that the inhibition of endogenous TNF[alpha] blocks both the induction and expression of the shock-induced deficit, suggesting a necessary role for TNF[alpha] in mediating the inhibition of spinal learning. Conversely, Experiment 3 was designed to test the sufficiency for TNF[alpha] in producing a learning deficit. I found that treatment with exogenous TNF[alpha] undermined spinal learning in a dose-dependent fashion, whether given immediately, or 24 hours prior to testing. Experiment 4 demonstrated that the long-term TNF[alpha]-induced deficit is mediated by TNF[alpha] receptor activity, as a TNF inhibitor given prior to testing blocked the expression of this deficit. As TNF[alpha] has been shown to be predominantly of glial origin, I next assessed the role that glia play in the TNFa-induced deficit. Experiment 5 showed that inhibiting glial metabolism prior to TNFa treatment blocked the capacity for TNFa to produce a long-term deficit…
  note: by John Russell Huie.
  note: "Major Subject: Psychology"
  note: Electronic resource.
  note: Doctor of Philosophy Texas A&M University 2010 http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8594
  note: Includes bibliographical references.
  note: Text (Dissertation)
  subject:
    topic: Major psychology
  subject:
    topic: Instrumental learning
  subject:
    topic: Cytokine
  subject:
    topic: Spinal cord
  subject:
    topic: Plasticity
  identifier: http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8594
  record info:
    record content source: TXA
    record creation date: 120312
    record change date: 20151202151732.0
    record identifier: in00002742454