Neural Regeneration Research ›› 2017, Vol. 12 ›› Issue (9): 1458-1464.doi: 10.4103/1673-5374.215256

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Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils

Jae-Chul Lee1, Jeong-Hwi Cho1, Tae-Kyeong Lee1, In Hye Kim1, Moo-Ho Won1, Geum-Sil Cho2, Bich-Na Shin3, In Koo Hwang4, Joon Ha Park5, Ji Hyeon Ahn5, Il Jun Kang6, Young Joo Lee7, Yang Hee Kim8   

  1. 1 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea
    2 Department of Pharmacology & Toxicology, Shinpoong Pharmaceutical Co., Ltd., Ansan, South Korea
    3 Department of Physiology, College of Medicine, Hallym University, Chuncheon, South Korea
    4 Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National
    University, Seoul, South Korea
    5 Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea
    6 Department of Food Science and Nutrition, Hallym University, Chuncheon, South Korea
    7 Department of Emergency Medicine, Seoul Hospital, College of Medicine, Sooncheonhyang University, Seoul, South Korea
    8 Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, South Korea
  • Received:2017-07-17 Online:2017-09-15 Published:2017-09-15
  • Contact: Moo-Ho Won, D.V.M., Ph.D. or Yang Hee Kim, M.D.,mhwon@kangwon.ac.kr or kyh1524@kangwon.ac.kr.
  • Supported by:

    This study was supported by the Biomedical Technology Development Program of the NRF funded by the Korean Government, MSIP (NRF-2015M3A9B6066835), and by the Bio-Synergy Research Project (NRF-2015M3A9C4076322) of the Ministry of Science, ICT and Future Planning through the National Research Foundation.

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Abstract:

Calbindin D-28K (CB), a Ca2+-binding protein, maintains Ca2+ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic insults. We investigated the effects of transient global cerebral ischemia on CB immunoreactivity as well as neuronal damage in the hippocampal formation under hyperthermic condition using immunohistochemistry for neuronal nuclei (NeuN) and CB, and Fluoro-Jade B histofluorescence staining in gerbils. Hyperthermia (39.5 ± 0.2°C) was induced for 30 minutes before and during transient ischemia. Hyperthermic ischemia resulted in neuronal damage/death in the pyramidal layer of CA1–3 area and in the polymorphic layer of the dentate gyrus at 1, 2, 5 days after ischemia. In addition, hyperthermic ischemia significantly decreaced CB immunoreactivity in damaged or dying neurons at 1, 2, 5 days after ischemia. In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia. Present findings indicate that the degree of reduced CB immunoreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.

Key words: nerve regeneration, hyperthermic condition, ischemia/reperfusion injury, subregions of hippocampus, delayed neuronal death, calbindin D-28k, neural regeneration