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Hypoxic damage of the cerebellum in 7-day-old rats. Ultrastructural and histochemical study

100%
Dambska M., Gajkowska B.
Acta Neurobiologiae Experimentalis
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2002
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vol. 62
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issue 1
45-49
EN
The damaging influence of hypoxia on the cerebellum in immature rats, which is still discussed, was investigated. Using material obtained in a modified Levine model for combined hypoxic-ischemic damage in 7-day-old rats, we examined changes in cerebellum submitted to hypoxia only. The results demonstrated classic features of hypoxic nervous tissue damage and calcium accumulation in mitochondria and endoplasmic reticulum. This was investigated using electron microscopy combined with the oxalate-pyroantimonate method. We propose that Ca2+ increases in endoplasmic reticulum and mitochondrial Ca2+ pools may be involved in damage-mediated mechanisms. These results support a role of calcium as a mechanism of cerebellar cell loss after this form of injury.
2
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Effect of 3-aminobenzamide on Bcl-2, Bax and AIF localization in hippocampal neurons altered by ischemia-reperfusion injury. The immunocytochemical study

100%
Strosznajder R., Gajkowska B.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 1
15-22
EN
Poly(ADP-ribose) polymerase plays an important role in cell survival and death. Our previous histological and ultrastructural studies showed that PARP inhibitor 3-aminobenzamide (3-AB) protected neurons against death after ischemia. In this study we investigated the effect of 3-AB on the localization and expression of apoptosis inducing factor (AIF) and on two proteins from Bcl-2 family: Bcl-2 and Bax in hippocampal area CA1, on the 4th day after 3 min of forebrain ischemia in gerbils. Our results indicated that after ischemia AIF is preferentially translocated from the mitochondria to the cytoplasm and to the nucleus. Intravenous administration of 3-AB (30 mg/kg b.w.) prevents AIF translocation to the nucleus. AIF was mainly seen in the structurally unchanged mitochondria and Golgi complex. Moreover, after 3-AB administration overexpression of Bcl-2 protein was observed in mitochondrial membranes, rough endoplasmatic reticulum, Golgi complex, nuclear envelopes, and also in cytoplasm and in nucleus. These data suggest that inhibition of PARP activity may have a beneficial effect on hippocampal neurons through overexpression of Bcl-2 protein and suppression of AIF translocation to the nucleus.
3
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Photochemically-induced vascular damage in brain cortex. Transmission and scanning electron microscopy study

81%
Gajkowska B., Frontczak-Baniewicz M., Gadomski R., Barskov I.
Acta Neurobiologiae Experimentalis
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1997
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vol. 57
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issue 3
203-208
EN
Morphological changes of microvessels of cerebral cortex were evaluated in a model of cerebral infarction initiated by a photochemical reaction. Rats were treated with intravenous injection of rose Bengal and irradiated from a halogen lamp source through an intact cranium to precipitate microvascular damage. Investigations in transmission and scanning electron microscopy revealed platelet aggregation on endothelial cells preceded by its early ultrastructural damage. Other typical microscopic features of brain ischaemic injury were present suggesting that the present method may be used as a model for investigating ischaemic brain damage. Since the photochemical activation of the rose Bengal dye results in formation of reactive oxygen species this model may be particularly useful to elucidate the role of free radical-mediated endothelial damage in the formation of microthrombi and blood-brain-barrier integrity.
4
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Neurotoxic effect of sodium tellurite in rat temporal lobe

81%
Gajkowska B., Smialek M., Porada D., Piotrowski P.
Acta Neurobiologiae Experimentalis
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1995
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vol. 55
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issue 3
221
5
Content available remote

Structure of cytomatrix and nuclear matrix revealed by embedment-free electron microscopy

81%
Gajkowska B., Cholewinski M., Gniadecki R.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 2
147-158
EN
Embedment-free electron microscopy (EFEM) is a new method which allows the visualisation of cytoskeleton in whole-mounted cells. In this study we employed EFEM to investigate the structure of cellular scaffolds in glioma C6 cell line. The cells were extracted with Triton X-100 that dissolves phospholipids in the membranes and removes most of cytoplasmic soluble proteins. The DNA and nuclear histones were removed with DNase I and high-salt buffer, respectively. The remaining cellular frameworks were temporary embedded in diethylene glycol distearate (DGD), sectioned and observed in transmission and scanning electron microscope after the removal of DGD. The predominant structure was the extensive meshwork of 10-20 nm filaments in the cytoplasm (cytomatrix) and 15-30 nm filaments in the nucleus (nuclear matrix). The 5 nm filaments, presumably corresponding to the actin filaments, were present in the cytomatrix, but not in the nuclear matrix. Moreover, the ultrathin (3 nm) filaments, connecting other cytoskeletal components were detected. Those are possibly identical with the previously described plectin filaments. For the first time we report the occurrence of ultrathin filaments in the nuclear matrix. Thus, in a addition to the well known cytoskeletal components (microtubules, intermediate filaments, actin microfilaments) EFEM showed a new type of filaments (the ultrathin filaments) in the cytomatrix and nuclear matrix. Further immunocytochemical studies are needed to determine the biochemical identity of the filaments observed in EFEM.
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