Puga, Denise Alejandra (2007-08). The opponent consequences of intermittent and continuous stimulation within the rat spinal cord. Master's Thesis. Thesis uri icon

abstract

  • A substantial body of work exists to suggest that brain and spinal mechanisms react differently to nociceptive information. The current experiments were design to identify parallels and differences in the way the spinal cord processes nociceptive information, as compared to intact animals. In addition, pharmacological manipulations were employed to identify the opioid receptors activated by continuous shock, and to decipher at what synaptic level (e.g. pre or post synaptically) intermittent shock affects the release of endogenous opioids. A common dependent variable was used in all experiments to assess changes in nociceptive reactivity, the tail-flick test. The results revealed that intermittent and continuous stimulation have an opponent relationship on nociceptive processing in the isolated spinal cord. Continuous stimulation (3, 25-s continuous 1.5 mA tail-shocks) induced an antinociceptive response that was attenuated by prior exposure to brief (80 ms) intermittent shock (Experiment 1). When intermittent shock was given after continuous shock, intermittent shock failed to attenuate continuous shock-induced antinociception (Experiment 2). The impact of intermittent shock on continuous-shock induced antinociception decayed after 24 hours (Experiment 3). Intermittent and continuous shock enhanced the antinociceptive consequences of a moderate dose of systemic morphine (5 mg/kg) (Experiment 4). Continuous shock-induced antinociception was attenuated by equal molar concentrations of CTOP (u opioid antagonist) and Nor-BNI (? opioid antagonist), but not naltrindole (? opioid antagonist) (Experiment 5). Intermittent shock failed to attenuate the antinociception induced by DAMGO (u opioid agonist) or Dynorphin A (? opioid agonist).
  • A substantial body of work exists to suggest that brain and spinal mechanisms
    react differently to nociceptive information. The current experiments were design to
    identify parallels and differences in the way the spinal cord processes nociceptive
    information, as compared to intact animals. In addition, pharmacological manipulations
    were employed to identify the opioid receptors activated by continuous shock, and to
    decipher at what synaptic level (e.g. pre or post synaptically) intermittent shock affects
    the release of endogenous opioids. A common dependent variable was used in all
    experiments to assess changes in nociceptive reactivity, the tail-flick test.
    The results revealed that intermittent and continuous stimulation have an
    opponent relationship on nociceptive processing in the isolated spinal cord. Continuous
    stimulation (3, 25-s continuous 1.5 mA tail-shocks) induced an antinociceptive response
    that was attenuated by prior exposure to brief (80 ms) intermittent shock (Experiment 1).
    When intermittent shock was given after continuous shock, intermittent shock failed to
    attenuate continuous shock-induced antinociception (Experiment 2). The impact of
    intermittent shock on continuous-shock induced antinociception decayed after 24 hours
    (Experiment 3). Intermittent and continuous shock enhanced the antinociceptive consequences of a moderate dose of systemic morphine (5 mg/kg) (Experiment 4).
    Continuous shock-induced antinociception was attenuated by equal molar concentrations
    of CTOP (u opioid antagonist) and Nor-BNI (? opioid antagonist), but not naltrindole (?
    opioid antagonist) (Experiment 5). Intermittent shock failed to attenuate the
    antinociception induced by DAMGO (u opioid agonist) or Dynorphin A (? opioid
    agonist).

publication date

  • August 2007