title: Effects of ischemic tolerance on mRNA levels of IP3R1, beta-actin, and neuron-specific enolase in hippocampal CA1 area of the gerbil brain.
abstract: Global cerebral ischemia induced to Mongolian gerbils by ligation of common carotid arteries (CCAs) is known to result in injury to the hippocampal CA1 region. In this study, we examined whether neuronal injury can be depicted by measuring levels of mRNA encoding inositol 1,4,5-trisphosphate receptor type 1 (IP3R1), neuron specific enolase (NSE) and beta-actin and whether these measurements can be use to assess ischemic tolerance. Gerbils were subjected either to cerebral ischemia induced by ligation of both CCAs for 5 min, or to an ischemic tolerance paradigm in which a 2 min ischemic preconditioning was performed 24 hr prior to the 5 min ischemia. At 48 hr after the 5 min ischemic insult, significant decreases in mRNA levels for IP3R1 (26%), NSE (38%) and beta-actin (50%) could be observed in the hippocampal CA1 region. Although levels of mRNA in the preconditioning group were decreased as compared to the sham control, the levels were significantly higher than those in the ischemic group. These results indicate the feasibility of using mRNA measurement as a parameter to assess cerebral ischemic damage. In addition, based on the differences in the decline in mRNA levels between the ischemia group and the preconditioned ischemia group, it can be concluded that this ischemic tolerance paradigm could offer partial protection (around 45%) against the injury due to the 5 min cerebral ischemic insult.
authors.affiliation: Biochemistry Department, University of Missouri, Columbia 65212, USA.
authors.forename: W
authors.initials: W
authors.lastname: Farwell
authors.forename: A
authors.initials: A
authors.lastname: Simonyi
authors.forename: H
authors.initials: H
authors.lastname: Scott
authors.forename: J P
authors.initials: JP
authors.lastname: Zhang
authors.forename: V
authors.initials: V
authors.lastname: Carruthers
authors.forename: R
authors.initials: R
authors.lastname: Madsen
authors.forename: J
authors.initials: J
authors.lastname: Johnson
authors.forename: G Y
authors.initials: GY
authors.lastname: Sun
mesh_terms: D000199:Actins / Q000096:biosynthesis*; D000818:Animals; D001921:Brain / Q000098:blood supply / Q000378:metabolism; D015220:Calcium Channels / Q000096:biosynthesis*; D005849:Gerbillinae; D006624:Hippocampus / Q000098:blood supply* / Q000378:metabolism*; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D053496:Inositol 1,4,5-Trisphosphate Receptors; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D019194:Ischemic Preconditioning; D009928:Organ Specificity; D010751:Phosphopyruvate Hydratase / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000096:biosynthesis; D018160:Receptors, Cytoplasmic and Nuclear / Q000096:biosynthesis*; D013997:Time Factors; D014158:Transcription, Genetic
chemical_list: D000199:Actins; D015220:Calcium Channels; D053496:Inositol 1,4,5-Trisphosphate Receptors; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D015544:Inositol 1,4,5-Trisphosphate; D010751:Phosphopyruvate Hydratase