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Enhancement of [3H]D-aspartate release during ischemia like conditions in rat hippocampal slices:source of excitatory amino acids

100%
Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
63-70
EN
Ischemic neuronal injury is supposed to be caused in part by the extracellular accumulation of excitatory amino acids (EAA). Neurotransmitter and metabolic EAA can be released from synaptic vesicles and cytoplasm of neurones and glial cells. In this study the release of the glutamate analogue [3H]D-aspartate (3[H]D-ASP), loaded into 500 mugm slices of rat hippocampus, was investigated. The efflux of the label was measured during anoxic - aglycemic ("ischemic") and normoxic K+ depolarization. To identify the pools from which [3H]D-ASP is released we have estimated its calcium dependence and the effects of inhibitors of: (1) Na+ - dependent transporter of amino acids (100 mugM L-trans-pyrrolidine-2,4-dicarboxylic acid /L-trans-PDC/), (2) sodium channel (1 mugM tetrodotoxin TTX), and (3) anion channel (1mM furosemide). [3H]D-ASP released upon normoxic depolarization was 40% inhibited by TTX,nearly 40% by L-trans-PDC and over 50% by furosemide. The "ischemic" release was in 40% calcium dependent, completely TTX independent and in approximately 50% blocked by furosemide treatment. Our data suggest that EAA accumulated in the synaptic cleft during ischemia are mainly released from the cytosolic compartment by mechanisms wich are connected with the ischemic increase of extracellular potassium concentration.
2
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Changes of Ca2+/calmodulin - dependent protein kinase-II after transient ischemia in gerbil hippocampus

81%
Zalewska T., Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
41-48
EN
Transient cerebral ischemia induces, besides delayed neurodegeneration in selected brain structures, a number of early responses which may mediate ischemic injury/repair processes. Here we report that 5 min exposure to cerebral ischemia in gerbils induces a rapid inhibition and subsequent translocation of Ca (2+)/calmodulin-dependent protein kinase II (CaMKII). These changes were partially reversible during a 24 h post-ischemic recovery. Concomitantly the total amount of the enzyme protein, as revealed by Western blotting (alfa- -subunit specific), remained stable. This is consistent with our previous hypothesis, that the mechanism of ischemic CaMKII down-regulation involves a reversible posttranslational modification-(auto)phosphorylation, rather then the degradation of enzyme protein. The effectiveness of known modulators of postischemic outcome in counteracting CaMKII inhibition was tested. Three of these drugs, namely dizocilpine (MK-801), N-nitro-L-arginine methyl ester (L-NAME) and gingkolide (BN52021), all significantly attenuated the enzyme response to ischemia, whereas an obvious diversity in the time-course of their actions implicates different mechanisms involved.
3
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Phosphorylation of Protein Kinase C substrate proteins in rat hippocampal slices - effect of calpain inhibition

81%
Domanska-Janik K., Zablocka B., Zalewska T., Zajac H.
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vol. 58
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issue 4
247-252
EN
Incubation of the acutely dissected rat hippocampal slices in calcium-containing media resulted in spontaneous activation-translocation of classical PKC isoforms and their subsequent (especially g- type) proteolytic degradation. These changes were blocked by calpain inhibitor MDL 28 170 in 100 mM concentration. Rat hippocampal slices were metabolically prelabelled with 32Pi and stimulated with NMDA/glycine, depolarization or phorbol dibutyrate (PDBu) treatment. The basal phosphorylation of specific PKC substrates (MARCKS, neuromodulin and neurogranin) was significantly reduced in non-stimulated slices by MDL pretreatment. In contrast, only the slices where calpain activity was inhibited responded to further NMDA or phorbol dibutyrate stimulation by a substantial increase of PKC-dependent protein phosphorylation. It is concluded that the PKC phosphorylation system is severely affected by non-specific activation and a subsequent, calpain-dependent proteolysis in the acutely prepared hippocampal slices. Calpain inhibition by 100 mM MDL partially prevented these changes and increased stimulus-dependent phosphorylation of PKC-specific protein substrates.
4
Content available remote

Interrelations between nuclear-factor kappa B activation, glial response and neuronal apoptosis in gerbil hippocampus after ischemia

81%
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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