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Trimethilin-induced plastic neuronal changes in rat hippocampus are accompanied be astrocytic trophic activity

100%

Koczyk D., Skup M., Zaremba M., Oderfeld-Nowak B.

Acta Neurobiologiae Experimentalis

1996

vol. 56

issue 1

237-241

Partial deafferentation of the hippocampus due to trymethyltin (TMT) intoxication has been reported to induce plastic rearrangements of neuronal elements but the factors that direct these responses are unknown. To assess the possible involvement of nerve growth factor (NGF) in the phenomenon we evaluated the presumable changes in the expression pattern of NGF immunoreactivity (NGF-IR) in rat hippocampus 21 days after administration of TMT (8 mg/kg, i.p.) when reactive changes are fully developed. Immunolabelling for TrkA known to mediate biological effects of NGF and for GFAP to identify astroglial cells as a one of presumed source of postinjury produced factors was carried out on adjacent sections to establish the relation between expression of these proteins. In control hippocampus NGF-IR and TrkA-IR were localized in neurons and/or nueropil. After exposure to TMT remarkable non-neuronal expression of both proteins was observed. The distribution pattern of NGF, TrkA and GFAP overlapped suggesting that reactive asrtocytes may not only produce NGF but also may become responsive to this neurotrophin. Zones of extensive NGF and TrkA astroglial expression corresponded to areas of axonal-dendritic rearrangements reported earlier. That data suggest that astroglia-derived trophic activity may be involved in neuronal plastic events associated with treatment with TMT.

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

2001

vol. 61

issue 1

45-51

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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2 Acta Neurobiologiae Experimentalis

1 2001

1 1996

1 Bronisz-Kowalczyk A.

1 Domanska-Janik K.

1 Koczyk D.

1 Oderfeld-Nowak B.

1 Skup M.

1 Zablocka B.

1 Zajac H.

1 Zaremba M.

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Trimethilin-induced plastic neuronal changes in rat hippocampus are accompanied be astrocytic trophic activity

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