CD200 Change Is Involved in Neuronal Death in Gerbil Hippocampal CA1 Field Following Transient Forebrain Ischemia and Postischemic Treatment with Risperidone Displays Neuroprotection without CD200 Change

International Journal of Molecular Sciences

JoonHa Park¹  DaeWon Kim²  Tae-Kyeong Lee³  MyoungCheol Shin⁴  JunHwi Cho⁴  Young-Myeong Kim⁵  Jae-Chul Lee⁶  Hyejin Sim⁶  Bora Kim⁶  Moo-Ho Won⁶  Choong-Hyun Lee⁷  JiHyeon Ahn⁸ 

[1] Department of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju, Gyeongbuk 38066, Korea;Department of Biochemistry and Molecular Biology and Research Institute of Oral Sciences, College of Dentistry, Gangnung-Wonju National University, Gangneung, Gangwon 25457, Korea;Department of Biomedical Science and Research, Institute for Bioscience and Biotechnology, Hallym University, Chuncheon, Gangwon 24252, Korea;Department of Emergency Medicine, Institute of Medical Sciences, Kangwon National University Hospital, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24289, Korea;Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341, Korea;Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341, Korea;Department of Pharmacy, College of Pharmacy, Dankook University, Cheonan, Chungnam 31116, Korea;Department of Physical Therapy, College of Health Science, Youngsan University, Yangsan, Gyeongnam 50510, Korea;

关键词: CD200;    transient ischemia;    pyramidal neurons;    DND;    microglia;    GABAergic interneurons;   

DOI  :  10.3390/ijms22031116

来源: DOAJ

【 摘 要 】

It has been reported that CD200 (Cluster of Differentiation 200), expressed in neurons, regulates microglial activation in the central nervous system, and a decrease in CD200 expression causes an increase in microglial activation and neuronal loss. The aim of this study was to investigate time-dependent changes in CD200 expression in the hippocampus proper (CA1, 2, and 3 fields) after transient forebrain ischemia for 5 min in gerbils. In this study, 5-min ischemia evoked neuronal death (loss) of pyramidal neurons in the CA1 field, but not in the CA2/3 fields, at 5 days postischemia. In the sham group, CD200 expression was found in pyramidal neurons of the CA1 field, and the immunoreactivity in the group with ischemia was decreased at 6 h postischemia, dramatically increased at 12 h postischemia, decreased (to level found at 6 h postischemia) at 1 and 2 days postischemia, and significantly increased again at 5 days postischemia. At 5 days postischemia, CD200 immunoreactivity was strongly expressed in microglia and GABAergic neurons. However, in the CA3 field, the change in CD200 immunoreactivity in pyramidal neurons was markedly weaker than that in the CA1 field, showing there was no expression of CD 200 in microglia and GABAergic neurons. In addition, treatment of 10 mg/kg risperidone (an atypical antipsychotic drug) after the ischemia hardly changed CD200 immunoreactivity in the CA1 field, showing that CA1 pyramidal neurons were protected from the ischemic injury. These results indicate that the transient ischemia-induced change in CD200 expression may be associated with specific and selective neuronal death in the hippocampal CA1 field following transient forebrain ischemia.

【 授权许可】

Unknown