Immunohistochemical Study of Glucose Transporters 1 and 3 in the Mouse Hippocampus after Kainic Acid Treatment.
- Author:
Seung Jin KWAG
1
;
Kyu Hong KIM
;
Hyun Joon KIM
;
Sang Soo KANG
;
Gyeong Jae CHO
;
Wan Sung CHOI
;
Gu Seob ROH
Author Information
1. Department of Anatomy, Medical Research Center for Neural Dysfunction, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 660-751, Korea. anaroh@gnu.kr
- Publication Type:Original Article
- Keywords:
Kainic acid;
Seizure;
Glucose transporter;
Hippocampus;
Mouse
- MeSH:
Animals;
Benzoxazines;
Brain;
Caspase 3;
Cell Death;
Endothelial Cells;
Energy Metabolism;
Glial Fibrillary Acidic Protein;
Glucose;
Glucose Transport Proteins, Facilitative;
Hippocampus;
Immunohistochemistry;
Kainic Acid;
Mice;
Neurons;
Paraventricular Hypothalamic Nucleus;
Proteins;
Seizures;
Viola
- From:Korean Journal of Anatomy
2008;41(3):213-221
- CountryRepublic of Korea
- Language:English
-
Abstract:
Seizure activity increases glucose utilization within the brain in response to neuronal injury. In this study, we investigated the expression of two brain glucose transporter (GLUT) proteins, GLUT1 and GLUT3, in the mouse hippocampus after kainic acid (KA) treatment. Forty-eight hours after KA (30 mg/kg) injection, mice were sacrificed and a histological evaluation of KA-treated hippocampus revealed cell death using cresyl violet staining and immunohistochemistry for caspase-3. In KA-treated hippocampus, reactive astrocytic changes were confirmed by increased immunoreactivity of glial fibrillary acidic protein (GFAP). Enhanced GLUT1-positive endothelial cells were present in the hippocampus after KA treatment. However, GLUT3-positive neurons were not localized to the KAtreated hippocampus. In particular, although GLUT-3 was not expressed in the hippocampus, pronounced GLUT3- positive cells were observed in the hypothalamic paraventricular nucleus (PVN), which controls energy metabolism. Thus, these results indicate that changes in endothelial GLUT1 and neuronal GLUT3 levels in response to neural injury may play important roles in neuroprotection against brain excitotoxicity.
