Difference in transient ischemia-induced neuronal damage and glucose transporter-۱ immunoreactivity in the hippocampus between adult and young gerbils

Publish Year: 1395
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:

JR_IJBMS-19-5_009

تاریخ نمایه سازی: 30 مهر 1400

Abstract:

Objective(s): The alteration of glucose transporters is closely related with the pathogenesis of brain edema. We compared neuronal damage/death in the hippocampus between adult and young gerbils following transient cerebral ischemia/reperfusion and changes of glucose transporter-۱(GLUT-۱)-immunoreactive microvessels in their ischemic hippocampal CA۱ region. Materials and Methods: Transient cerebral ischemia was developed by ۵-min occlusion of both common carotid arteries. Neuronal damage was examined by cresyl violet staining, NeuN immunohistochemistry and Fluoro-Jade B histofluorescence staining and changes in GLUT-۱ expression was carried out by immunohistochemistry. Results: About ۹۰% of pyramidal neurons only in the adult CA۱ region were damaged after ischemia/reperfusion; in the young, about ۵۳ % of pyramidal neurons were damaged from ۷ days after ischemia/reperfusion. The density of GLUT-۱-immunoreactive microvessels was significantly higher in the young sham-group than that in the adult sham-group. In the ischemia-operated-groups, the density of GLUT-۱-immunoreactive microvessels was significantly decreased in the adult and young at ۱ and ۴ days post-ischemia, respectively, thereafter, the density of GLUT-۱-immunoreactive microvessels was gradually increased in both groups after ischemia/reperfusion. Conclusion: CA۱ pyramidal neurons of the young gerbil were damaged much later than that in the adult and that GLUT-۱-immunoreactive microvessels were significantly decreased later in the young. These data indicate that GLUT-۱ might differently contribute to neuronal damage according to age after ischemic insults.

Keywords:

CA۱ region , Delayed neuronal death , Ischemia/reperfusion injury Pyramidal neurons , Young gerbil

Authors

Seung Min Park

Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Jae-Chul Lee

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Bai Hui Chen

Department of Physiology, College of Medicine, Hallym University, Chuncheon ۲۰۰-۷۰۲, South Korea

Bich-Na Shin

Department of Physiology, College of Medicine, Hallym University, Chuncheon ۲۰۰-۷۰۲, South Korea

Jeong Hwi Cho

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

In Hye Kim

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Joon Ha Park

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Moo-Ho Won

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Ji Hyeon Ahn

Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon ۲۰۰-۷۰۲, South Korea

Hyun-Jin Tae

Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon ۲۰۰-۷۰۲, South Korea

Myoung Cheol Shin

Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Chan Woo Park

Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Jun Hwi Cho

Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

Hui Young Lee

Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon ۲۰۰-۷۰۱, South Korea

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