PT  - JOURNAL ARTICLE
AU  - Changsheng Li
AU  - Ya Yang
AU  - Sufang Liu
AU  - Huaqiang Fang
AU  - Yong Zhang
AU  - Orion Furmanski
AU  - John Skinner
AU  - Ying Xing
AU  - Roger A. Johns
AU  - Richard L. Huganir
AU  - Feng Tao
TI  - Stress Induces Pain Transition by Potentiation of AMPA Receptor Phosphorylation
AID  - 10.1523/JNEUROSCI.2130-14.2014
DP  - 2014 Oct 08
TA  - The Journal of Neuroscience
PG  - 13737--13746
VI  - 34
IP  - 41
4099  - http://www.jneurosci.org/content/34/41/13737.short
4100  - http://www.jneurosci.org/content/34/41/13737.full
SO  - J. Neurosci.2014 Oct 08; 34
AB  - 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.