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Behavioral evaluation of ischemic damage to CA1 hippocampal neurons: Effects of preconditioning

100%
Duszczyk M., Ziembowicz A., Gadamski R., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
311-319
EN
In Mongolian gerbils, global forebrain ischemia induces enhanced locomotor activity and the disruption of nest building immediately after the insult, followed by damage to hippocampal neurons developing 3 days later. Preconditioning by a brief episode of sublethal ischemia induces the protection of CA1 hippocampal neurons against a lethal ischemic insult. We examined how preconditioning with 2-min ischemia affects disturbances in the nest building behavior and locomotor activity induced by the injurious 3-min ischemia. Morphological examination confirmed that preconditioning significantly reduced neuronal damage in CA1 evoked by injurious ischemia. Behavioral studies demonstrated that preconditioning reduced the locomotor hyperactivity and latency in nest building after test ischemia, in comparison to sham or naive animals. The results indicate that the nest building test and measurement of locomotor activity may be used for an early in vivo prediction of the extent of ischemic brain damage and tolerance induced by ischemic preconditioning.
2
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Ischemia-related alteration of GABAA-operated chloride channel properties in gerbil hippocampus and cerebral cortex

88%
Strosznajder J., Koladkiewicz I., Chalimoniuk M., Samochocki M.
Acta Neurobiologiae Experimentalis
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1998
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vol. 58
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issue 2
95-102
EN
The properties of GABA-gated chloride (Cl^-) channels in ischemia-reperfusion injury were studied by determination of the binding and dissociation kinetics of a specific Cl^- channel ligand, tert-butylbicyclophosphoro[^35S]thionate (TBPS) and by determination of ^36Cl^- uptake in the presence of the GABAA receptor agonist, muscimol. Four days after ischemia a small but insignificant decrease of [^35S]TBPS binding to synaptic plasma membranes (SPM) was observed in the hippocampus and cerebral cortex as compared to control. The effect of ischemia was larger and statistically significant after the first and second month of reperfusion, constituting 20% inhibition of [^35S]TBPS binding to SPM of sham-operated gerbils. On the other hand, the half-life of fast phase [^35S]TBPS dissociation four days after ischemia was markedly diminished by about 40%-50% as compared to its control value and persisted during the first and second month of reperfusion in the hippocampal SPM. A similar but less potent reduction of the half-life of the fast phase of [^35S]TBPS dissociation (about 30% versus control) appeared one and two months after ischemia in cerebral cortex SPM. One month after ischemia muscimol-stimulated ^36Cl^- uptake into cerebral cortex synaptoneurosomes was lowered as compared with control uptake, but remained statistically insignificant in the whole range of muscimol concentrations tested. Our results indicated that ischemia-reperfusion injury significantly decreases opening time of GABAA receptor-gated Cl^- channels in the hippocampus and cerebral cortex, which may lower the hyperpolarization ability of this receptor complex leading to an imbalance between excitatory and inhibitory neurotransmitter pathways in these brain areas, and in consequence to neuronal dysfunction or degeneration.
3
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Interrelations between nuclear-factor kappa B activation, glial response and neuronal apoptosis in gerbil hippocampus after ischemia

75%
Domanska-Janik K., Bronisz-Kowalczyk A., Zajac H., Zablocka B.
Acta Neurobiologiae Experimentalis
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2001
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vol. 61
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issue 1
45-51
EN
Spatial and temporal relations between transcriptional factor NFkB activation and glia reaction in gerbil hippocampus after transient cerebral ischemia has been studied. Activation of protein binding to NFkB consensus oligonucleotide was determined by electrophoretic mobility gel shift assay (EMSA) in homogenates from dorsal (DP- an equivalent of CA1 sector) and abdominal (AbP- containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of NFkB binding was observed exclusively in DP as early as 3 h after ischemia and at this time that response preceded any other morphological signs of postischemic tissue injury. This early enhancement of NFkB binding was followed by microglia activation visualized in CA1 pyramidal region at 24 h of recovery by histochemical staining with lectin from Ricinus communis (RCA-120). Simultaneously, only a moderate increase of immunostaining against glial fibrillary acidic protein (GFAP) was observed homogeneously in all parts of hippocampus. This uniform pattern of astrogliosis was preserved until postischemic day 3-4, when apoptotic DNA fragmentation in CA1 pyramidal neurons had been clearly documented by TUNEL staining. At this period however, continuous elevation of NFkB binding in DP corresponded with similar response manifested also in AbP of the hippocampus. These results evidence a preferential NFkB involvement in an early microglia activation in the apoptogenic CA1 sector, although its role in a later astrocytic response to ischemia could not be neglected too.
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