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GLIAL ENDOTHELIN/NITRIC OXIDE SYSTEM PARTICIPATES IN HIPPOCAMPUS CA1 NEURONAL DEATH OF SHRSP FOLLOWING TRANSIENT FOREBRAIN ISCHAEMIA
Author(s) -
Yamashita Kimihiro,
Kataoka Yasufumi,
Yamashita Yasuko S.,
Himeno Akihiko,
Tsutsumi Keisuke,
Niwa Masami,
Taniyama Kohtaro
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02915.x
Subject(s) - hippocampus , microglia , forebrain , medicine , nitric oxide , endothelin receptor , endocrinology , nitric oxide synthase , ischemia , programmed cell death , neuroscience , receptor , chemistry , biology , central nervous system , inflammation , apoptosis , biochemistry
Summary 1. When delayed neuronal death occurred in the hippocampus CA1 pyramidal cell layer of stroke‐prone spontaneously hypertensive rats (SHRSP) at 4 and 7 days after a 10 min bilateral carotid occlusion and reperfusion, intense endothelin‐1 (ET‐1)‐ and ET‐3‐like immunoreactivities became evident in astrocytes in the damaged hippocampus CA1 subfields. 2. We also observed that microglia equipped with an ET b receptor aggregated within the CA1 pyramidal cell layer with neuronal death. 3. There was a dramatic increase in nitric oxide synthase (NOS) activity in astrocytes and microglia in the damaged hippocampus CA1 subfields. 4. Thus, the possibility that microglia with the ET b receptor are activated to produce NO, a neurotoxic factor, by astrocytic ET‐1 and ET‐3 produced in response to transient forebrain ischaemia would have to be considered.