Immunohistochemical Study of the Expression of pERK1/2 Protein in the Forebrains of Adult Rodents Following Hypoxia-ischemia injury.
- Author:
Yong Jae HAN
1
;
Hun Cheol AHN
;
Jae Hwang PARK
;
Su Jin YOO
Author Information
1. Department of Emergency Medicine, Wonkwang University School of Medicine, Korea. ysoojin@wmc.wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
Hypoxia-Ischemia;
Brain;
Extracellular Signal-Regulated MAP Kinases;
Hippocampus
- MeSH:
Adult;
Brain;
Carotid Artery, Common;
Dendrites;
Extracellular Signal-Regulated MAP Kinases;
Hippocampus;
Humans;
Neurons;
Prosencephalon;
Respiration;
Rodentia
- From:Journal of the Korean Society of Emergency Medicine
2008;19(3):313-321
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The purpose of this study was to evaluate spatiotemporal evaluation of pERK1/2 protein expression in the forebrain following hypoxic-ischemic (HI) injury in adult Sprague-Dawley rats. METHODS: HI injury was induced by occlusion of the bilateral common carotid artery (CCA) and respiration with 5% O2 hypoxic gas for 8 minutes, followed by unilateral release of CCA. RESULTS: Immunoreactivity for pERK1/2 protein in the bilateral cortex began to increase at 2 hours, reached peak levels at 6 hours, and then decreased by 24 hours after HI injury. In a cortical neuron, the expression of pERK1/2 protein was observed in all cellular components and processes including dendrites, cell body and nuclei at 6 hours, but persisted only in the cell body by 24 hours after HI injury. Temporal changes in the immunoreactivity for pERK1/2 protein in the hippocampus was very similar to that of the cortex following HI injury. In contrast, the temporal changes in the cellular distribution of pERK12 protein in hippocampal neurons was largely different from that of the cortex following HI injury. CONCLUSION: The results of the present study suggest that HI injury causes an early activation of ERK1/2 signaling with a differential cellular distribution of pERK1/2 protein among different forebrain structures. Further study needs to be done in order to elucidate a possible role of ERK1/2 signaling for neural damage in the adult rodent HI model.
