Stress induces pain transition by potentiation of AMPA receptor phosphorylation

Changsheng Li, Y. Yang, Sufang Liu, Huaqiang Fang, Yong Zhang, Orion Furmanski, John Skinner, Ying Xing, Roger A. Johns, Richard L. Huganir, Feng Tao

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


Chronic postsurgical pain is a serious issue in clinical practice. After surgery, patients experience ongoing pain or become sensitive to incident, normally nonpainful stimulation. The intensity and duration of postsurgical pain vary. However, it is unclear how the transition from acute to chronic pain occurs. Here we showed that social defeat stress enhanced plantar incision-induced AMPA receptor GluA1 phosphorylation at the Ser831 site in the spinal cord and greatly prolonged plantar incision-induced pain. Interestingly, targeted mutation of the GluA1 phosphorylation site Ser831 significantly inhibited stress-induced prolongation of incisional pain. In addition, stress hormones enhanced GluA1 phosphorylation and AMPA receptor-mediated electrical activity in the spinal cord. Subthreshold stimulation induced spinal long-term potentiation in GluA1 phosphomimetic mutant mice, but not in wild-type mice. Therefore, spinal AMPA receptor phosphorylation contributes to the mechanisms underlying stress-induced pain transition.

Original languageEnglish (US)
Pages (from-to)13737-13746
Number of pages10
JournalJournal of Neuroscience
Issue number41
StatePublished - Oct 8 2014


  • AMPA receptor phosphorylation
  • Pain transition
  • Stress

ASJC Scopus subject areas

  • Neuroscience(all)


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