Growing pains: the cytoskeleton as a critical regulator of pain plasticity

Neuron. 2003 Aug 14;39(4):577-9. doi: 10.1016/s0896-6273(03)00500-2.

Abstract

Inflammatory mediators act on peripheral sensory neurons to produce pain and hypersensitivity after tissue injury. In this issue of Neuron, Dina et al. report that inflammatory mediators, such as epinephrine and prostaglandins, appear to couple to specific G protein-coupled receptor signaling pathways through plastic interactions with the cytoskeleton.

Publication types

  • Comment
  • Review

MeSH terms

  • Animals
  • Cytoskeleton / physiology*
  • Dinoprostone / metabolism
  • Epinephrine / metabolism
  • Neuronal Plasticity / physiology*
  • Neurons, Afferent / physiology
  • Nociceptors / physiology
  • Pain / physiopathology*
  • Receptors, Chemokine / physiology
  • Signal Transduction / physiology*

Substances

  • Receptors, Chemokine
  • Dinoprostone
  • Epinephrine