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Peer-reviewedCC BY-NC-ND 4.0In Vivo

Increased GluA1 Expression, c-Fos Activation, and MAP2 Loss During Early Cerebral Ischemia-reperfusion

  • HYOIN HWANG1,2
  • JUNGHEE PARK1,3
  • HYEKYOUNG SHIN2
  • YOONYOUNG CHUNG2
  • DONGJOON KIM4
  • YONGHYUN JUN2,5
5 affiliations
  1. 1Institute of Well-Aging Medicare & Chosun University G-LAMP Project Group, Chosun University, Gwang-ju, Republic of Korea
  2. 2Department of Anatomy, School of Medicine, Chosun University, Gwang-ju, Republic of Korea
  3. 3Department of Biochemistry and Molecular Biology, Chosun University, Gwang-ju, Republic of Korea
  4. 4Department of Anesthesiology and Pain Medicine, Chosun University Hospital, Gwang-ju, Republic of Korea
  5. 5The Institute of Medical Science, Chosun University, Gwang-ju, Republic of Korea
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Abstract

Background/Aim: The disruption of excitatory and inhibitory neurotransmission is a key pathological event in ischemia/reperfusion injury. However, the temporal relationship among glutamatergic activation, inhibitory responses, and neuronal activity in the early phase of reperfusion remains unclear. The present study investigated changes in GluA1 signaling, GABAA receptor α1 expression, neuronal activation, and neuronal integrity following transient cerebral ischemia.

Materials and Methods: Transient focal cerebral ischemia was induced in male C57BL/6 mice by middle cerebral artery occlusion (MCAO). Mice were sacrificed immediately following ischemia (0 h) or 3 h after reperfusion. The expression levels of phosphorylated GluA1 (pGluA1), total GluA1, and GABAA receptor α1 in the ipsilateral cortex were analyzed by western blotting. Neuronal activation and integrity were evaluated using immunofluorescence staining for c-Fos and MAP2, respectively.

Results: The expression levels of pGluA1 and total GluA1 increased following MCAO and remained elevated after 3 h of reperfusion, whereas the pGluA1/total GluA1 ratio did not differ significantly among the experimental groups. GABAA receptor α1 expression did not differ significantly among the groups, although it tended to be higher after reperfusion. Immunofluorescence revealed a focal reduction in MAP2 immunoreactivity in the reperfusion group, while no obvious changes were observed immediately after ischemia. In addition, c-Fos immunoreactivity increased in both the ischemic and reperfusion groups compared with the sham group.

Conclusion: Early cerebral ischemia-reperfusion is characterized by progressive activation of GluA1 signaling, increased neuronal activity, and the onset of neuronal injury. GABAA receptor α1 expression showed a non-significant tendency to be higher after reperfusion, and the functional significance of this trend remains uncertain. These findings indicate that early cerebral ischemia-reperfusion is associated with altered GluA1 expression, increased neuronal activity, and early neuronal injury.

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Cite

BibTeXRIS
BibTeX
@article{hwang2026increased,
  title = {{Increased GluA1 Expression, c-Fos Activation, and MAP2 Loss During Early Cerebral Ischemia-reperfusion}},
  author = {HYOIN HWANG and JUNGHEE PARK and HYEKYOUNG SHIN and YOONYOUNG CHUNG and DONGJOON KIM and YONGHYUN JUN},
  journal = {In Vivo},
  year = {2026},
  month = oct,
  doi = {10.21873/invivo.14489},
  url = {https://doi.org/10.21873/invivo.14489},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Increased GluA1 Expression, c-Fos Activation, and MAP2 Loss During Early Cerebral Ischemia-reperfusion
AU  - HYOIN HWANG
AU  - JUNGHEE PARK
AU  - HYEKYOUNG SHIN
AU  - YOONYOUNG CHUNG
AU  - DONGJOON KIM
AU  - YONGHYUN JUN
PY  - 2026
DA  - 2026/10/29
JO  - In Vivo
DO  - 10.21873/invivo.14489
UR  - https://doi.org/10.21873/invivo.14489
AB  - Background/Aim: The disruption of excitatory and inhibitory neurotransmission is a key pathological event in ischemia/reperfusion injury. However, the temporal relationship among glutamatergic activation, inhibitory responses, and neuronal activity in the early phase of reperfusion remains unclear. The present study investigated changes in GluA1 signaling, GABAA receptor α1 expression, neuronal activation, and neuronal integrity following transient cerebral ischemia.  Materials and Methods: Transient focal cerebral ischemia was induced in male C57BL/6 mice by middle cerebral artery occlusion (MCAO). Mice were sacrificed immediately following ischemia (0 h) or 3 h after reperfusion. The expression levels of phosphorylated GluA1 (pGluA1), total GluA1, and GABAA receptor α1 in the ipsilateral cortex were analyzed by western blotting. Neuronal activation and integrity were evaluated using immunofluorescence staining for c-Fos and MAP2, respectively.  Results: The expression levels of pGluA1 and total GluA1 increased following MCAO and remained elevated after 3 h of reperfusion, whereas the pGluA1/total GluA1 ratio did not differ significantly among the experimental groups. GABAA receptor α1 expression did not differ significantly among the groups, although it tended to be higher after reperfusion. Immunofluorescence revealed a focal reduction in MAP2 immunoreactivity in the reperfusion group, while no obvious changes were observed immediately after ischemia. In addition, c-Fos immunoreactivity increased in both the ischemic and reperfusion groups compared with the sham group.  Conclusion: Early cerebral ischemia-reperfusion is characterized by progressive activation of GluA1 signaling, increased neuronal activity, and the onset of neuronal injury. GABAA receptor α1 expression showed a non-significant tendency to be higher after reperfusion, and the functional significance of this trend remains uncertain. These findings indicate that early cerebral ischemia-reperfusion is associated with altered GluA1 expression, increased neuronal activity, and early neuronal injury.
SN  - 0258-851X
SN  - 1791-7549
ER  -