title: Nitric oxide produced during ischemia is toxic but crucial to preconditioning-induced ischemic tolerance of neurons in culture.
abstract: The present study investigated the roles of nitric oxide (NO) in preconditioning (PC)-induced neuronal ischemic tolerance in cortical cultures. Ischemia in vitro was simulated by subjecting cultures to both oxygen and glucose deprivation (OGD). A sublethal OGD (PC) significantly increased the survival rate of neurons when cultures were exposed to a lethal OGD 24 h later. Both the inhibition of nitric oxide synthase (NOS) and scavenging of NO during PC significantly attenuated the PC-induced neuronal tolerance. In addition, exposure to an NO donor emulated the PC. In contrast, the inhibition of NOS and the scavenging of NO during lethal OGD tended to increase the survival rate of neurons. This study suggested that NO produced during ischemia was fundamentally toxic, but critical to the development of PC-induced neuronal tolerance.
authors.affiliation: Laboratory of Biomedical Control, Research Institute for Electronic Science, Hokkaido University, Sapporo, Japan. kawahara@bmc.es.hokudai.ac.jp
authors.forename: Koichi
authors.initials: K
authors.lastname: Kawahara
authors.forename: Junji
authors.initials: J
authors.lastname: Yanoma
authors.forename: Motoki
authors.initials: M
authors.lastname: Tanaka
authors.forename: Takayuki
authors.initials: T
authors.lastname: Nakajima
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Kosugi
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D007150:Immunohistochemistry; D019194:Ischemic Preconditioning; D009569:Nitric Oxide / Q000502:physiology* / Q000633:toxicity; D051381:Rats
chemical_list: D009569:Nitric Oxide