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

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 ins...

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Published in:Neural regeneration research Vol. 12; no. 9; pp. 1458 - 1464
Main Authors: Lee, Jae-Chul, Cho, Jeong-Hwi, Lee, Tae-Kyeong, Kim, In Hye, Won, Moo-Ho, Cho, Geum-Sil, Shin, Bich-Na, Hwang, In Koo, Park, Joon Ha, Ahn, Ji Hyeon, Kang, Il Jun, Lee, Young Joo, Kim, Yang Hee
Format: Journal Article
Language:English
Published: India Medknow Publications and Media Pvt. Ltd 01-09-2017
Medknow Publications & Media Pvt. Ltd
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea%Department of Pharmacology & Toxicology, Shinpoong Pharmaceutical Co., Ltd., Ansan, South Korea%Department of Physiology, College of Medicine, Hallym University, Chuncheon, South Korea%Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul, South Korea%Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea%Department of Food Science and Nutrition, Hallym University, Chuncheon, South Korea%Department of Emergency Medicine, Seoul Hospital, College of Medicine, Sooncheonhyang University, Seoul, South Korea%Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, South Korea
Medknow Publications & Media Pvt Ltd
Wolters Kluwer Medknow Publications
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Summary: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 inves- tigated 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 neu- ronal 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 immunoreac- tivity 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 immu- noreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.
Bibliography:nerve regeneration; hyperthermic condition; ischemia/reperfusion injury; subregions of hippocampus;delayed neuronal death; calbindin D-28k; neural regeneration
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 inves- tigated 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 neu- ronal 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 immunoreac- tivity 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 immu- noreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.
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These authors contributed equally to this study.
Author contributions: The design, implementation and evaluation of the study were carried out by all the authors. All authors approved the final version of the paper.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.215256