Wyniki wyszukiwania

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Effect of allopregnanolone on D-[3H]-aspartate release and [3H]-glutamate uptake in the hippocampus of kainate-treated mice

100%

Leskiewicz M., Budziszewska B., Jaworska-Feil L., Lason W.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 2

In order to determine whether the status epilepticus leads to alterations in the neurosteroid effect on excitatory amino acid transmission, we studied the influence of allopregnanolone on aspartate release and glutamate uptake in mouse hippocampus at various times after kainate administration. No significant differences in the K+-stimulated D-[3H]-aspartate release from the hippocampi of saline- and kainate-treated mice were observed; however, that parameter tended to fall in tissues collected 1h after kainate administration. Allopregnanolone significantly attenuated the K+-stimulated D-[3H]-aspartate release from the hippocampi of control animals, as well at 24 h and 7 days after kainate injection; in contrast it did not affect amino acid release from the hippocampi collected 1 h after kainate administration. Kainate administration had no effect on [3H]-glutamate uptake after 1 and 24 h, but elevated that parameter on day 7. Allopregnanolone (10 and 100 µM) did not affect [3H]-glutamate uptake in control and kainate-treated mice. In conclusion, the present study indicates a loss of the inhibitory effect of allopregnanolone on the potasium-stimulated D-[3H]-aspartate release from mouse hippocampus during the kainate-induced status epilepticus; moreover, it excludes involvement of this neurosteroid in the regulation of hippocampal [3H]-glutamate uptake in both control and kainate-treated mice.

2

The protective role of astroglia in the early period of experimental lead toxicity in the rat

80%

Struzynska L.

Acta Neurobiologiae Experimentalis

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2000

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tom 60

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nr 2

Although the clinical manifestations of lead (Pb) neurotoxicity are documented, the subcellular mechanisms of its action are still an open question. The purpose of this study was to assess the function of nerve ending particles after acute lead exposure and to investigate whether it exerts a toxic effect on astroglial functions. The studies were performed using the rodent model of acute lead toxicity. Cellular fractions were used in biochemical measurements - synaptosomes and glial plasmalemmal vesicles (GPV). Since a procedure for the isolation of the fraction of astroglial origin has been developed, it becomes possible to investigate lead-astroglia interactions after in vivo exposure. It is of importance because most of the studies concerning lead toxicity were performed using astroglial culture systems. It was found that the uptake of glutamate (Glu) to the synaptosomes was lowered and KCl-dependent release was increased, suggesting the impairment of glutamatergic transmission leading to the elevation of extracellular amino acid concentration. In contrast, glutamate uptake to the GPV fraction was significantly elevated. The activity of the marker enzyme - glutamine synthetase (GS) was also significantly increased in the GPV fraction. The activation of glial functions suggest a regulatory role for these cells in the early period of acute lead toxicity.

3

The effect of glutamate uptake inhibitors on hippocampal evoked potentials in vitro

80%

El-Sherif Y., Singh N., Khan T., Wieraszko A.

Acta Neurobiologiae Experimentalis

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1999

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tom 59

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nr 2

Ograniczanie wyników

2 Acta Neurobiologiae Experimentalis

1 Journal of Physiology and Pharmacology

1 Budziszewska B.

1 El-Sherif Y.

1 Jaworska-Feil L.

1 Khan T.

1 Lason W.

1 Leskiewicz M.

1 Singh N.

1 Struzynska L.

1 Wieraszko A.

1 2002

1 2000

1 1999

Effect of allopregnanolone on D-[3H]-aspartate release and [3H]-glutamate uptake in the hippocampus of kainate-treated mice

The protective role of astroglia in the early period of experimental lead toxicity in the rat

The effect of glutamate uptake inhibitors on hippocampal evoked potentials in vitro