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Role of calcium in glutamate-mediated toxicity: mechanisms of calcium fluxes in rabbit hippocampus in vivo investigated with microdialysis

100%

Lazarewicz J. W., Salinska E.

Acta Neurobiologiae Experimentalis

1993

vol. 53

issue 1

3-13

Calcium ions are known to play a key role in the mechanism of excitotoxic and ischemic neuronal injury.< Hippocampal CA1 neurons> are selectively susceptible to this kind of damage. Although various have been identified in the hippocampal neurons, it is not clear what the main pathway for Ca?+ entry is during overexcitation. These studies were aimed to estimate a potential contribution of different types of calcium ionophores in calcium redistribution to hippocampal neurons in vivo.The local microdialysis technique, combined with the 45Ca?+ utilizing method was used to measure the changes in extracellular Ca?+ concentrations ([Ca?+]e) in the rabbit hippocampus in vivo, and to apply active substances directly to the hippocampus. The application of N-methyl-D-aspartate (NMDA) resulted in a large, dose-dependent decrease of [Ca?+]e, which was sensitive to APV and MK-801, but was only slightly reduced by and . The effect of high potassium medium was less pronounced and only slightly inhibited by nimodipine. However it was inhibited by 75% in the presence of MK-801 and then completely cancelled by nimodipine. To visualize the depolarization-induced calcium influx to hippocampal cells, KC1-induced cellular swelling and resulting shrinkage of the extracellular space, monitored with [U-14C]sucrose , was taken into account in calculating these data. These results indicate that calcium redistribution into hippocampal neurons through NMDA channels may highly exceed calcium fluxes in the hippocampus, attributable to a stimulation of the L-type voltage-sensitive calcium channels.

Effect of acute hepatic encephalopathy on [3H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2+

88%

Borkowska H., Oja S. S., Hilgier W., Saransaari P., Albrecht J.

Acta Neurobiologiae Experimentalis

2000

vol. 60

issue 1

1-7

Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KCl) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.

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2 Acta Neurobiologiae Experimentalis

1 2000

1 1993

1 Albrecht J.

1 Borkowska H.

1 Hilgier W.

1 Lazarewicz J. W.

1 Oja S. S.

1 Salinska E.

1 Saransaari P.

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Role of calcium in glutamate-mediated toxicity: mechanisms of calcium fluxes in rabbit hippocampus in vivo investigated with microdialysis

Effect of acute hepatic encephalopathy on [3H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2+