title: Regional differences in the rate of energy impairment after threshold level ischemia for induction of cerebral infarction in gerbils.
abstract: The development of infarction and/or selective neuronal death in the brain after transient cerebral ischemia depends on the severity of the ischemic episode. After transient cerebral ischemia of the threshold level for the induction of infarction, both changes evolve slowly in various postischemic regions. We examined the relationship of disturbances of energy metabolism to infarction and selective neuronal death in various regions of the postischemic brain subjected to two 10-min occlusions of the unilateral common carotid artery. Our results indicated that in various cerebral regions that developed infarction, the tissue ATP content, in parallel with the succinic dehydrogenase activity, fell to their lowest levels at different times over a 4-day period after circulation had been restored (earliest to latest: dorsolateral thalamus > dorsolateral caudate > chiasmal level cortex > hippocampal CA3 sector > hippocampal CA sector). In the cortex at the infundibular level, disseminated selective neuronal death developed over a 7-day period following restoration of circulation; it was accompanied by only a slight alteration in energy metabolism. The present results indicate that regional differences existed in the rate of energy impairment and evolving infarction in the postischemic gerbil brain. Energy impairment, in association with mitochondrial enzymatic dysfunction, seems to be indispensable for the delayed manifestation of cerebral infarction but not for disseminated selective neuronal death.
authors.affiliation: Department of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Yushima, Japan. kuroiwa@e-mail.ne.jp
authors.forename: T
authors.initials: T
authors.lastname: Kuroiwa
authors.forename: G
authors.initials: G
authors.lastname: Mies
authors.forename: D
authors.initials: D
authors.lastname: Hermann
authors.forename: Y
authors.initials: Y
authors.lastname: Hakamata
authors.forename: S
authors.initials: S
authors.lastname: Hanyu
authors.forename: U
authors.initials: U
authors.lastname: Ito
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002421:Caudate Nucleus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002544:Cerebral Infarction / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology*; D005849:Gerbillinae; D005947:Glucose / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006863:Hydrogen-Ion Concentration; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013788:Thalamus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors
chemical_list: D000255:Adenosine Triphosphate; D013385:Succinate Dehydrogenase; D005947:Glucose