Research Paper Volume 12, Issue 5 pp 4299—4321
Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex
- 1 School of Biomedical Engineering, Tianjin Medical University, Tianjin, China
- 2 Chinese Institute for Brain Research, Beijing (CIBR), Beijing, China
- 3 Department 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
- 4 Tianjin 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
- 5 Department of Physiology and Membrane Biology, University of California Davis School of Medicine, Sacramento, CA 95817, USA
- 6 Division of Neurodegenerative Disorders, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China
- 7 Research Institute of Neurology, General Hospital, Tianjin Medical University, Tianjin, China
received: December 6, 2019 ; accepted: February 5, 2020 ; published: March 9, 2020 ;https://doi.org/10.18632/aging.102881
How to Cite
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.
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.