Skip to main content

(NAS Colloquium) The Neurobiology of Pain (1999) / Chapter Skim
Currently Skimming:

Transcriptional and Posttranslational Plasticity and the Generation of Inflammatory Pain
Pages 7723-7730

The Chapter Skim interface presents what we've algorithmically identified as the most significant single chunk of text within every page in the chapter.
Select key terms on the right to highlight them within pages of the chapter.


From page 7723...
... This transcription-dependent potentiated system now displays an enhanced responsiveness to subsequent central sensitization-inducing inputs. Finally, the last state follows peripheral inflammation, where a combination of activity-dependent and signal molecule-mediated posttranslational and transcriptional changes in the sensory and dorsal horn neurons results in a fundamentally altered system, one in which the transduction sensitivity of the peripheral terminals is reduced (peripheral sensitization)
Read the entire page →
From page 7724...
... (B) C fiber inputs induce immediate posttranslational changes in the dorsal horn, resulting in central sensitization and altering basal sensitivity such that low intensity stimuli result in pain.
Read the entire page →
From page 7725...
... Nociceptive conduction. Voltage-gated sodium channels, which are responsible for the rising phase of the action potential and play a key role, with potassium channels, in determining the excitability of the sensory neurons, mediate conduction in nociceptors by transferring input from the peripheral nerve terminals to the spinal cord.
Read the entire page →
From page 7726...
... These transmitters/neuromodulators act on receptors and ion channels in the dorsal horn to activate protein kineses that phosphorylate membranebound NMDA and AMPA receptors and alter their functional properties, increasing membrane excitability and thereby eliciting central sensitization.
Read the entire page →
From page 7727...
... These changes include early posttranslational changes both in the peripheral terminals of nociceptors, altering transduction sensitivity (peripheral sensitization) , and in dorsal horn neurons secondary to activity in C fibers (central sensitization)
Read the entire page →
From page 7728...
... 4. Posttranslational changes in transduction mechanisms/ion channels at nociceptor peripheral terminals induced by inflammatory mediators increases sensitivity and reduces threshold (peripheral sensitization)
Read the entire page →
From page 7729...
... 4~. Apart from the increased sensitivity of the peripheral terminals of nociceptors on exposure to inflammatory mediators, which will result in an area of increased sensitivity to thermal and mechanical stimuli localized to the site of inflammation, any C fiber input activated at the time of or during inflammation will also initiate central sensitization.
Read the entire page →
From page 7730...
... (1991) Sensory Mechanisms of the Spinal Cord (Plenum, New York)
Read the entire page →

Key Terms

  • horn neurons
  • central sensitization
  • posttranslational changes
  • map kinase
  • transcriptional changes

  • basal sensitivity
  • fiber inputs
  • sensory neurons
  • sodium channels
  • peripheral sensitization

  • protein kinase
  • peripheral terminals
  • ion channels
  • dorsal root
  • kinase cascade

  • root ganglion
  • pain hypersensitivity
  • ttxr sodium
  • primary afferent
  • afferent neurons

  • inflammatory mediators
  • sodium current
  • peripheral stimuli
  • conditioning input
  • input basal

  • normally innocuous
  • signal molecules
  • primary sensory
  • noxious stimuli
  • mechanical stimuli


    • This material may be derived from roughly machine-read images, and so is provided only to facilitate research.
    More information on Chapter Skim is available.