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(NAS Colloquium) The Neurobiology of Pain (1999) / Chapter Skim
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Cellular Mechanisms of Neuropathic Pain, Morphine Tolerance, and Their Interactions
Pages 7731-7736

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From page 7731...
... A site of action involved in both hyperalgesia and morphine tolerance is in the superficial laminae of the spinal cord dorsal horn. These observations suggest that hyperalgesia and morphine tolerance may be interrelated at the level of the superficial laminae of the dorsal horn by common neural substrates that interact at the level of excitatory amino acid receptor activation and subsequent intracellular events.
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From page 7732...
... Thus, in addition to direct central sensitzation described above, the possible disinhibition resulting from the loss of function of spinal cord inhibitory interneurons may also contribute to central hyperexcitability after peripheral nerve injury and inflammation. Central Mechanisms Subserv~ng Morphine Tolerance.
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From page 7733...
... The major findings of this series of studies are (i) the incidence of dark neurons increased significantly within the spinal cord dorsal horn, particularly the superficial laminae I-II, of rats injected daily for 8 days with i.t.
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From page 7734...
... (iv) At the spinal cord level, it is likely, except in the presence of nociceptive input, that presynaptic elements release only small amounts of glutamate onto postsynaptic elements in the superficial laminae of the dorsal horn that contain NMDA receptors related to opioid tolerance, yet tolerance to opioids occurs in the absence of nociceptive input.
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From page 7735...
... 5. A proposed model for the excitotoxic formation of dark neurons in the dorsal horn of the spinal cord from peripheral nerve injury or repeated morphine administration.
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From page 7736...
... It should be noted that, although early treatment of pain after tissue injury and inflammation with opioids often provides satisfactory clinical pain relief, opioids alone offer little help for stopping the process of an evolving pathological pain state, because evidence presented in this article and elsewhere suggests that opioids alone could actually contribute to the development of neuronal plastic changes via interactions with NMDA receptors. It can be anticipated that our further understanding of neural mechanisms subserving hyperalgesia, opioid tolerance, and their interactions Proc.
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Key Terms

  • spinal cord
  • dorsal horn
  • morphine tolerance
  • nmda receptor
  • neuropathic pain

  • nmda receptors
  • opioid tolerance
  • rats receiving
  • nerve injury
  • pain states

  • excitatory amino
  • cord dorsal
  • neuronal plastic
  • amino acid
  • receptor activation

  • pathological pain
  • plastic changes
  • receptor antagonists
  • superficial laminae
  • intracellular events

  • subsequent intracellular
  • protein kinase
  • central nervous
  • pain syndromes
  • nociceptive input

  • cell death
  • opiate treatment
  • pkc translocation
  • cci model
  • peripheral nerve


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