title: C57BL/6 strain is most susceptible to cerebral ischemia following bilateral common carotid occlusion among seven mouse strains: selective neuronal death in the murine transient forebrain ischemia.
abstract: Rats and gerbils have been used widely to investigate the molecular mechanism of selective neuronal death following transient global ischemia. Recently, the availability of transgenic mice has enabled us to examine the involvement of specific gene products in various pathophysiological conditions. However, there has been only limited information about the experimental model of cerebral ischemia in mice, particularly in regard to selective neuronal death. We examined whether bilateral carotid occlusion produced global forebrain ischemia in seven common mouse strains including C57BL/6, ICR, BALB/c, C3H, CBA, ddY and DBA/2, based on neurological signs, histological findings and cortical microcirculatory as well as India ink perfusion patterns. The C57BL/6 strain was found to be the most susceptible among seven strains. All C57BL/6 mice died within 6 h after permanent bilateral carotid occlusion. After transient bilateral carotid occlusion for 20 min, more than 90% of C57BL/6 mice showed typical neurological signs such as torsion of the neck and rolling fits, and developed selective neuronal death in the hippocampus and caudoputamen. Hypothermia prevented the neuronal death. Visualization of brain vasculature by India ink perfusion indicated that the susceptibility of the mice after bilateral carotid occlusion depended mainly on the degree of anastomosis between carotid and basilar arteries. Our results showed the feasibility of investigating selective neuronal death in transgenic mice with simple temporary occlusion of both common carotid arteries, when those from the C57BL/6 strain or inbred transgenic mice from other strains with the C57BL/6 strain in a back-cross manner are used.
authors.affiliation: First Department of Internal Medicine, Osaka University Medical School, Suita, Japan.
authors.forename: G
authors.initials: G
authors.lastname: Yang
authors.forename: K
authors.initials: K
authors.lastname: Kitagawa
authors.forename: K
authors.initials: K
authors.lastname: Matsushita
authors.forename: T
authors.initials: T
authors.lastname: Mabuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Yagita
authors.forename: T
authors.initials: T
authors.lastname: Yanagihara
authors.forename: M
authors.initials: M
authors.lastname: Matsumoto
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications*; D002545:Brain Ischemia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D017536:Carotid Artery, Common; D016923:Cell Death; D002560:Cerebrovascular Circulation; D003097:Collateral Circulation; D004198:Disease Susceptibility; D002546:Ischemic Attack, Transient / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL / Q000502:physiology*; D008815:Mice, Inbred Strains; D009420:Nervous System / Q000503:physiopathology; D009474:Neurons / Q000502:physiology*; D016548:Prosencephalon / Q000098:blood supply