Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex

Yuanyuan Li, Ran Ding, Feifei Wang, Cuiping Guo, Aili Liu, Liangpeng Wei, Shiyang Yuan, Feng Chen, Shaowei Hou, Zengguang Ma, Yan Zhang, Robert H. Cudmore, Xiaochuan Wang, Hui Shen

Research output: Contribution to journalArticlepeer-review


Brain ischemia results from cardiac arrest, stroke or head trauma. The structural basis of rescuing the synaptic impairment and cortical dysfunctions induced in the stage of ischemic-reperfusion can occur if therapeutic interventions are applied in time, but the functional basis for this resilience remains elusive. Here, we explore the changes in cortical activity and a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) GluA1 subunit in spine (sGluA1) after transient ischemia-reperfusion in vivo for 28 days. Using in vivo two-photon microscopy in the mouse somatosensory cortex, we found that the average frequency of Ca2+ transients in the spine (there was an unusual synchrony) was higher after 15 min of ischemia-reperfusion. In addition, the transient ischemia-reperfusion caused a reflective enhancement of AMPARs, which eventually restored to normal. The cortical hyperactivity (Ca2+ transients) and the increase in AMPARs were successfully blocked by an NMDA receptor antagonist. Thus, the increase of AMPARs, cortical hyperactivity and the unusual synchrony might be the reason for reperfusion injury after short-term transient ischemia.

Original languageEnglish (US)
Pages (from-to)4299-4321
Number of pages23
Issue number5
StatePublished - Mar 15 2020


  • AMPA receptor
  • Ca transients
  • Dendritic spine
  • Transient ischemia-reperfusion
  • somatosensory cortex

ASJC Scopus subject areas

  • Aging
  • Cell Biology


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