Pyramidal neurons surviving in the cornus ammonis 1 region of the hippocampus were evaluated 72 h after reperfusion, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) histochemistry, caspase-3 and superoxide dismutase (SOD)-2 immunohistochemistries, and Western blottings were performed, and object placement tests were carried out. 
The mean number of intact hippocampal cornus ammonis 1 (CA1) pyramidal neurons in rats subjected to cerebral ischemia without any pretreatment was 17+/-5 (neurons/mm+/-S.D.) 6 weeks after the ischemia; naïve, non-ischemic rats had 177+/-5 neurons/mm.
We measured the effects of isoflurane and sevoflurane on cornus ammonis 1 (CA1) pyramidal cells in rat hippocampal slices subjected to 10 min of hypoxia (95% nitrogen 5% carbon dioxide) and 60 min of recovery.
Severe transient forebrain ischemia causes selective neuronal death in the hippocampal cornus ammonis 1 region. We tested the hypothesis that fimbria-fornix deafferentation can provide long-term protection to cornus ammonis 1 neurons and modulate neurogenesis following ischemia. At 7 days after ischemia, 73%+/-14% of cornus ammonis 1 neurons were damaged, while deafferentation reduced the injury to 36%+/-17% of cornus ammonis 1 neurons. 6 to 11 cells/section in normal or sham stroke group), with very few terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling-stained cells adjacent to the hippocampal cornus ammonis 1. The results indicate that fimbria-fornix deafferentation provides long-term neuroprotection in cornus ammonis 1 following forebrain ischemia and promotes neurogenesis after ischemic insults..
Three sets of rat dorsal and ventral hippocampus slices were prepared: 1) transverse slices for examining a) the expression of the AMPA (GluRA, GluRB, GluRC) and NMDA (NR1, NR2A, NR2B) subunits mRNA using in situ hybridization, b) the protein expression of NR2A and NR2B subunits using Western blotting, and c) by using quantitative autoradiography, c(1)) the specific binding of the AMPA receptor agonist [ (3)H]AMPA and c(2)) the specific binding of the NMDA receptor antagonist [ (3)H]MK-801, 2) longitudinal slices containing only the cornus ammonis 1 (CA1) region for performing [ (3)H]MK-801 saturation experiments and 3) transverse slices for electrophysiological measures of NMDA receptor-mediated excitatory postsynaptic potentials.
OGD-induced neuronal death, in both the cornus ammonis 1 (CA1) and the dentate gyrus regions, peaked the first day after ischemia.
The ectopic expression of ACTH (1-24 fragments) immunoreactive neurons in the cornus ammonis 1 (CA1) region of hippocampus and hilar region of the dentate gyrus 1 day after the ischemic insult was observed.
-
[ View All ]
