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1
Content available remote

Strychnine antagonizes GABA-evoked 36 Cl?uptake in membrane vesicles from rat and rabbit cerebral cortex

100%
Puka M., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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1993
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vol. 53
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issue 4
511-516
2
Content available remote

Modulation of NMDA receptor - mediated release of [3h}arachidonate in hippocampal slices of immature rats

100%
Salinska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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1995
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vol. 55
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issue 1
11-21
EN
Using superfusion with albumin-containing medium of hippocampal and striatal slices of adult and developingrats at postnatal days(PND) 7-10, prelabelled with [3H]arachidonic acid ([3H]AA) we detected N-methyl-D-aspartate (NMDA) evoked release to the superfusion medium of radiolabelld material, 70% of which was associated with arachidonic acid (AA) and its metabolite.[3H[AA release was much more pronounced in PND 7-10 rats than in adults, and the response to NMDA in the hippocampal slices exceed the reactions in the striatal slices.The subsequent experiments, emplyoing only hippocampal slices of PND 7-10 rats, demonstrated that NMDA-stimulated [3H]AA release was dose-depended in the micromolar range,was sensitive to NMDA receptor antagonists, and wasinhibited in calcium-free medium and the presence of quinacrine.[3H]AA release induced by 100 ?M NMDA was not significantly inhibited by magnesium but was completly blocked by 7 Cl-kynurenic acid and ifenprodil (both antagonists 100 ?M).The sulfhydryl reducing reagent dithiothreitol induced [3H]AA release; this response was sensitive to NMDA receptor antagonists.These data indicate that the NMDA induced, calcium triggered, and phospholipides A2 depended AA release is highly pronounced in the developing rat hippocampus.NMDA receptors mediating AA release in the hippocampus of PND 7-10 rats are subject to glycine, polyamine and redox modulationn, but they show low sensitivity to Mg2+ inhibition.
3
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Excitotoxic neuronal injury in chronic homocysteine neurotoxicity studied in vitro: The role of NMDA and group I metabotropic glutamate receptors

100%
Zieminska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
301-309
EN
Elevated homocysteine is a risk factor in cardiovascular diseases and neurodegeneration. Among the putative mechanisms of homocysteine-evoked neurotoxicity, disturbances in methylation processes and NMDA receptor-mediated excitotoxicity have been suggested. Our previous studies demonstrated that group I metabotropic glutamate receptors along with NMDA receptors participate in acute homocysteine-induced neuronal damage. In this study, using propidium iodide staining, we tested whether the same mechanism may mediate chronic homocysteine neurotoxicity. Our results confirmed that the application of D,L-homocysteine in micromolar concentrations for 3 days induces neurodegeneration in primary cultures of cerebellar granule neurons. Uncompetitive NMDA receptor antagonist MK-801, and mGlu1 or mGlu5 receptor antagonists (LY367385 and MPEP, respectively), given alone provided very limited neuroprotection. However, simultaneous application of the NMDA receptor antagonists MK-801, memantine or amantadine and MPEP almost completely prevented chronic homocysteine neurotoxicity. These findings suggest a novel therapeutic strategy to combat neurodegeneration induced by hyperhomocysteinemia comprising a combination of antagonists of group I metabotropic glutamate receptors and NMDA receptors.
4
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Nicotinamide and 1-methylnicotinamide reduce homocysteine neurotoxicity in primary cultures of rat cerebellar granule cells

81%
Slomka M., Zieminska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 1
1-9
EN
Nicotinamide is an important cofactor in many metabolic pathways and a known neuroprotective substance, while its methylated product, 1-methylnicotinamide, is a suspected neurotoxin. Homocysteine is a risk factor in Alzheimer's disease and neurodegeneration, causing inhibition of methylation processes and inducing excitotoxicity. In this study, using primary cultures of rat cerebellar granule cells and propidium iodide staining, we investigated the neurotoxicity of nicotinamide and 1-methylnicotinamide, and their neuroprotective potential in acute and sub-acute homocysteine neurotoxicity. Our results demonstrated that nicotinamide and 1-methylnicotinamide applied for 24 h to cultures at concentrations of up to 25 mM had no effect on neuronal viability. Moreover, nicotinamide at concentrations of 5?20 mM and 1-methylnicotinamide at 1?10 mM applied to cells 24 h before, and for 24 h after an acute 30 min application of 25 mM D,L homocysteine, reduced neuronal damage. 1-Methylnicotinamide at concentrations of 250 and 500 ?M showed neuroprotective activity during a sub-acute 24-h exposure to 2.5 mM D,L-homocysteine, while 5 and 25 mM nicotinamide also evoked neuroprotection. These findings do not support suggestions that 1-methylnicotinamide may act as an endogenous neurotoxic agent; rather, they indicate the neuroprotective ability of nicotinamide and 1-methylnicotinamide in homocysteine neurotoxicity. The exact mechanisms of this neuroprotection are unclear and require further investigation.
5
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Behavioral evaluation of ischemic damage to CA1 hippocampal neurons: Effects of preconditioning

81%
Duszczyk M., Ziembowicz A., Gadamski R., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
311-319
EN
In Mongolian gerbils, global forebrain ischemia induces enhanced locomotor activity and the disruption of nest building immediately after the insult, followed by damage to hippocampal neurons developing 3 days later. Preconditioning by a brief episode of sublethal ischemia induces the protection of CA1 hippocampal neurons against a lethal ischemic insult. We examined how preconditioning with 2-min ischemia affects disturbances in the nest building behavior and locomotor activity induced by the injurious 3-min ischemia. Morphological examination confirmed that preconditioning significantly reduced neuronal damage in CA1 evoked by injurious ischemia. Behavioral studies demonstrated that preconditioning reduced the locomotor hyperactivity and latency in nest building after test ischemia, in comparison to sham or naive animals. The results indicate that the nest building test and measurement of locomotor activity may be used for an early in vivo prediction of the extent of ischemic brain damage and tolerance induced by ischemic preconditioning.
6
Content available remote

Effects of caffeine on NMDA-evoked 45Ca2+ release in the rat dentate gyrus in vivo

81%
Alaraj M., Kosinska I., Lazarewicz J. W.
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vol. 58
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issue 4
239-246
EN
Caffeine in 10-2 M concentration per se activates ryanodine receptors (RyR) in vitro, thereby increasing the intracellular concentration of Ca2+ ([Ca2+]i). In general opinion, caffeine applied in vivo in much lower doses does not affect [Ca2+]i in neurones. However, it was recently demonstrated that caffeine in low concentrations in vitro potentiates evoked Ca2+ release in neurones via RyR. Microdialysis of the rat dentate gyrus (DG), combined with measurement of 45Ca2+ efflux, has been used in our laboratory to study in vivo NMDA-evoked calcium induced calcium release (CICR) via RyR. The aim of the present microdialysis study was to investigate in vivo effects of caffeine, applied systemically in a pharmacologically-relevant dose, and locally in the dialysis medium in very high concentration, on the NMDA-evoked CICR in DG neurones. To ensure steady brain concentration of caffeine, its systemic (i.p.) administration in a dose of 40 mg/kg was followed by a continuous i.p. infusion of 80 mg/kg/min and application of 0.4 mM caffeine in the dialysis medium. The results demonstrated that in the rat DG, local administration of 50 mM caffeine significantly stimulates a spontaneous 45Ca2+ efflux and its release induced by 5 mM NMDA. However, systemic administration of caffeine had no effect on spontaneous and NMDA-induced 45Ca2+ release in the rat DG, which supports the view that caffeine, applied in vivo, even in high doses, does not influence CICR in brain neurones.
7
Content available remote

Preconditioning reduces hypoxia-evoked alterations in glutamatergic Ca2+ signaling in rat cortex

81%
Semenov D. G., Samoilov M. O., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 2
169-179
EN
The aims of this study were (1) to characterize calcium signaling in rat cortex induced by repeated in vitro application of the glutamatergic agonists L-glutamate, NMDA, AMPA and DHPG, (2) to analyze the influence of transient severe hypobaric hypoxia (180 Torr) administered in vivo on calcium responses to stimulation of glutamate receptors by their agonists, and (3) to evaluate the effects of preconditioning with intermittent mild hypobaric hypoxia (360 Torr), 24 h before the severe hypoxia, on these Ca2+ responses. Intracellular Ca2+ dynamics was studied using the fluorescent probes fura-2 and chlortetracycline to monitor free and bound calcium (Cai and Cab), respectively. In control cortical slices, application of L-glutamate, NMDA and AMPA induced concomitant increases in Cai and Cab, reflecting Ca2+ influx and its intracellular accumulation in neurons. DHPG, an agonist of group I mGlu receptors induced a decrease in Cab accompanied by a rise in Cai levels, indicating Ca2+ mobilization. In cortical slices collected 24 h after severe hypoxia, the responses of Cab to glutamate administration were increased, DHPG-induced shifts were reversed, the increase in Cab after the first application of AMPA was reduced, while after the second, Cab rises were potentiated, and the increases in Cab evoked by NMDA application were slightly suppressed. The alterations of responses in Cab to the selective agonists were completely prevented by preconditioning with mild hypoxia. Our results suggest that protection of normal glutamatergic calcium signaling contributes to tolerance to hypoxia induced by preconditioning.
8
Content available remote

N-metyl-D-aspartate-induced 45Ca(2+) release fom pre-labelled adult rat hippocampus in vivo

81%
Lazarewicz J. W., Rybkowski W., Puka-Sundvall M., Hagberg H.
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9
Content available remote

Local nimodipine application improves early functional recovery in the rabbit hippocampus after 15-min global cerebral ischemia

81%
Lazarewicz J. W., Pluta R., Puka M., Salinska E.
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10
Content available remote

NMDA receptors and nitric oxide regulate prostaglandin D2 synthesis in the rabbit hippocampus in vivo

52%
Lazarewicz J. W., Salinska S. E., Salinska E., Stafiej S. A., Stafiej A., Ziembowicz Z. A., Ziembowicz A., Zieminska Z. E., Zieminska E.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 4
427-435
EN
The aim of this in vivo microdialysis study was to characterise the regulation of prostaglandin D2 (PgD2) synthesis by NMDA receptors in the rabbit hippocampus in relation to changes in extracellular Ca2+ concentration ([Ca2+]e) and nitric oxide (NO) levels. Samples of dialysate were analysed for changes in PgD2 concentration, in [Ca2+]e and in the level of NO. The results demonstrated that a 20-min pulse application of 0.1 - 2.5 mM NMDA via a microdialysis probe induced a prolonged stimulation of PgD2 release that was sensitive to competitive NMDA receptor antagonists. An inhibitor of voltage-sensitive Na+ channels, tetrodotoxin, did not influence this effect but significantly suppressed basal PgD2 production, whereas a NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), prevented NMDA-evoked NO release and inhibited NMDA-induced PgD2 release in an L-arginine-sensitive manner. NO donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside, stimulated PgD2 release. NMDA-evoked decrease in [Ca2+]e was insensitive to TTX and L-NAME. These results demonstrate an in vivo NMDA receptor-mediated modulation of PgD2 synthesis in the brain, in which NO participates.
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