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Microglia with an Endothelin ET B Receptor Aggregate in Rat Hippocampus CA1 Subfields Following Transient Forebrain Ischemia
Author(s) -
Yamashita Kimihiro,
Niwa Masami,
Kataoka Yasufumi,
Shigematsu Kazuto,
Himeno Akihiko,
Tsutsumi Keisuke,
NakanoNakashima Mihoko,
SakuraiYamashita Yasuko,
Shibata Shigeki,
Taniyama Kohtaro
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.63031042.x
Subject(s) - hippocampus , microglia , forebrain , receptor , ischemia , medicine , endocrinology , neuroscience , biology , endothelin receptor , central nervous system , inflammation
We examined endothelin (ET) receptors in the hippocampus CA1 subfields of stroke‐prone spontaneously hypertensive rats subjected to a 10‐min bilateral carotid occlusion and reperfusion. When delayed neuronal death had occurred in the pyramidal cell layer at 7 days after transient forebrain ischemia, the quantitative receptor autoradiographic method we used revealed a dramatic increase in number of 125 I‐ET‐1 binding sites in the hippocampus CA1 subfields. The highest number of de novo binding sites appeared in the area corresponding anatomically to the pyramidal cell layer with neuronal death. These binding sites were characteristically the ET B receptor. The de novo 125 I‐ET‐1 binding was mainly present on microglia aggregating with a high density in the damaged pyramidal cell layer. As ET‐1‐ and ET‐3‐like immunoreactivities were highly expressed within astrocytes in damaged neural tissue, the possibility that microglia with the ET B receptor are activated to participate in the pathophysiology of ischemia‐related neural tissue damage by astrocytic ET‐1 and ET‐3 produced in response to transient forebrain ischemia would have to be considered.