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Research Paper|Volume 12, Issue 5|pp 4299—4321

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

Yuanyuan Li1, Ran Ding2, Feifei Wang1, Cuiping Guo3, Aili Liu1, Liangpeng Wei1, Shiyang Yuan1, Feng Chen1, Shaowei Hou1, Zengguang Ma1, Yan Zhang4, Robert H. Cudmore5, Xiaochuan Wang3,6, Hui Shen1,7
  • 1School of Biomedical Engineering, Tianjin Medical University, Tianjin, China
  • 2Chinese Institute for Brain Research, Beijing (CIBR), Beijing, China
  • 3Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
  • 4Tianjin Key Laboratory of Retinal Function and Diseases, Tianjin Medical University Eye Hospital, Eye Institute and School of Optometry and Ophthalmology, Tianjin Medical University, Tianjin, China
  • 5Department of Physiology and Membrane Biology, University of California Davis School of Medicine, Sacramento, CA 95817, USA
  • 6Division of Neurodegenerative Disorders, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China
  • 7Research Institute of Neurology, General Hospital, Tianjin Medical University, Tianjin, China
Received: December 6, 2019Accepted: February 5, 2020Published: March 9, 2020
https://doi.org/10.18632/aging.102881

Copyright © 2020 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.