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1

Common mechanisms of interacellular calcium release by TBBPA and thapsigargin in cultured neurons

100%
Ziemianska E., Stafiej A., Lazarewicz J.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Tetrabromobisphenol A (TBBPA) is a brominated flame retardant and the environmental toxin affecting the brain. The molecular mechanisms of the TBBPA-induced neurotoxicity are still unclear although recent studies suggest a role of calcium imbalance. It has been hypothesized that TBBPA may act as an intracellular calcium releaser from the stores in endoplasmic reticulum. To verify this hypothesis in the present study we examined changes in the intracellular calcium homeostasis induced by TBBPA, and their pharmacological modulation. Experiments were performed using an in vitro model of the primary cultures of rat cerebellar granule cells at 7th day in vitro. To evaluate TBBPA neurotoxicity, the cells were exposed for 30 min to TBBPA, and neuronal viability was tested after 24 h with propidium iodide staining. Changes in calcium homeostasis were characterized using the calcium-sensitive fluorescent probe fluo-3. The results demonstrated that TPPBA in concentrations exceeding 5 µM triggered rise in the intracellular calcium level, which was sensitive to inhibitors of ryanodine receptors 2.5 µM bastadin 10 with 200 µM ryanodine, but not to 2ABP, which inhibits IP3 receptors. The same features were disclosed for the effects of thapsigargin, that is a recognized inhibitor of the calcium pump SERCA and a well known calcium releaser. TPPBA in the concentration-dependent manner in the range of 2.5 - 100 µM induced severe neurotoxicity. The toxic effect of TPPBA in concentrations up to 10 - 15 µM was insensitive to antagonists of ryanodine receptors, bastadin 10 with ryanodine. Collectively, these results indicate that TBBP-A like thapsigargin is a calcium releaser destabilizing the ryanodine receptors, however this effect does not explain the mechanism of TBBPA neurotoxicity. This work was supported by the MNiSW grant N N401 024635.
2

TRP channels participare in memory formation in passive avoidance task in one day old chicks

100%
Salinska E., Stafiej A., Slomka M.
Acta Neurobiologiae Experimentalis
|
2015
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tom 75
|
nr Supl.
BACKGROUND AND AIMS: Influx of calcium ions (Ca2+) into neurons after stimulation of glutamate receptors is a crucial step in intracellular cascade of memory formation. Recent findings showed the existence of additional mechanism involved in intracellular Ca2+ increase and triggered not by external signal but by internal signals like increase of Ca2+ within the cell and activation of G protein coupled receptors. We are talking here about transient receptor potential (TRP) channels. The aim of our study was to investigate the participation of TRP channels, especially TRPC and TRPV in intracellular mechanisms engaged in memory consolidation. METHODS: The model of passive avoidance task on one day old chicks was used. Chicks were injected with TRP channels antagonist SKF96365 and three different concentrations of 2-APB, the inhibitor of IP3 receptors, which in small concentrations inhibits also TRP channels. The injections were made at different times before and after training, to find the most effective time of interference. RESULTS: We found that injection of all antagonists immediately after training resulted in task amnesia when tested 24 h later. The amnesic effect of injection of SKF96365 or 2-APB immediately after training was tested at different times. It appeared that SKF96365 injection resulted in constant amnesia that manifested 1.5 h after training, whereas amnesia after injection of 2-APB was observed as early as 30 min after training. The effect of application of TRP channels antagonist SKF96365 on memorizing of the task in comparison with the effects of mGluR1 and mGlR5 antagonists showed similarities when memory was tested 2 h and 24 h training. CONCLUSIONS: Our results show that inhibition of TRP channels results in disturbance in memory formation and that inhibition of both TRP channels and IP3 receptors using small concentrations of 2-APB has a strong impact on this process.
3

Pharmacological profiles of NMDA-induced eicosanoid release in rabbit hippocampus in vivo

100%
Zieminska E., Salinska E., Stafiej A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1995
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tom 55
|
nr 5
4

Complex mechanisms of tetrabromobisphenol A neurotoxicity in primary cultures of rat cerebellar granule cells

100%
Zieminska E., Stafiej A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Tetrabromobisphenol A (TBBPA) is a brominated flame retardant considered as the environmental toxin affecting the brain. The exact molecular mechanisms of the TBBPA-induced neurotoxicity are unclear, however recent studies suggest a role of the NMDA receptor-mediated excitotoxicity and/or of calcium imbalance. To verify this hypothesis in the present study we examined relation between toxicity of TBBPA applied to cultured neurons at the micro molar concentration range and activation of the NMDA receptors as well as changes in the intracellular calcium homeostasis, oxidative stress and a decrease in the mitochondrial membrane potential. Experiments were performed using an in vitro model of the primary cultures of rat cerebellar granule cells at 7th day in vitro. To evaluate TBBPA neurotoxicity, the cells were exposed for 30 min to TBBPA, and neuronal viability was tested after 24 h with propidium iodide staining. Changes in calcium homeostasis were characterized by measuring 45Ca uptake and increases in fluorescence of calcium-sensitive probe fluo-3. Changes in the mitochondrial membrane potential and in free radical production were evaluated using the fluorescent probes rhodamine 123 and DCF, respectively. The results demonstrated that TPPBA in the concentration-dependent manner in the range of 25 - 100µM induced severe neurotoxicity. TBBPA in concentrations exceeding 5 µM triggered rise in the intracellular calcium level, which was sensitive to inhibitors of ryanodine receptors 2.5 µM bastadin 10 with 200 µM ryanodine, but not to 2ABP, which inhibits IP3 receptors. TBBPA in concentrations above 25µM activated 45Ca uptake, which was sensitive to uncompetitive NMDA receptor antagonist 0.5 µM MK-801. Moreover we observed accumulation of the reactive oxygen species and a drop in the mitochondrial membrane potential evoked by TBBPA applied at micro molar concentrations. The toxic effect of TPPBA in concentrations up to 10 - 15 µM was insensitive to antagonists of NMDA receptors and ryanodine receptors, MK-801 and bastadin 10 with ryanodine, respectively. This points to a role of the mechanism of TBBPA neurotoxicity other than excitotoxicity and calcium imbalance. Tentatively we identify it as the oxidative stress. Collectively, these data point to complexity of the mechanisms of toxic effects of TBBPA. Depending of TBBPA concentrations they comprise oxidative stress, the release of calcium from ryanodie sensitive stores in endoplasmic reticulum and activation of NMDA receptors. This work was supported by the Polish MNiSW grant N N401 024635.
5

Is the NMDA receptor involved in neurotoxicity of pvp-coated silver nanoparticles? Study on primary cultures of cerebellar granule cells

100%
Zieminska E., Stafiej A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Silver nanoparticles (NAg) possess antibacterial properties thus are widely used in many applications in medicine, life sciences and biotechnology. Nanoparticles can be found in vertebrate brain, but little is known about their neurotoxicity. The aim of this study was to investigate how NAg can contribute to neuronal cell death. In the study primary cultures of rat cerebellar granule cells (CGC) were used. We tested hypothesis concerning the role of glutamatergic NMDA receptors in NAg-evoked neurotoxicity. In our study changes in intracellular calcium (Ca2+) homeostasis, uptake of 45Ca2+, reactive oxygen species (ROS) production, mitochondrial membrane potential and cells viability were investigated. We used commercially available 0.2% polyvinylpyrrolidone (PVP)-coated NAg <100 nm. To avoid sedimentation and agglomeration, before application to the CGC culture, NAg were sonicated with fetal calf serum. NAg were applied in concentration 2.5–75 µg/ml for 10, 30 min or 24 h, depending on experiment. As a pharmacological tool 0.5 µM MK801, a noncompetitive inhibitor of NMDA receptor, was used. After 10 min incubation in the presence of 25–75 µg/ ml NAg dose dependent increase of 45Ca2+ concentration was observed in neurons. This increase was comparable to that evoked by 100 µM glutamate and was completely abolished by MK801. Using fluorescent intracellular calcium indicator fluo3 we observed increase in intracellular calcium level by 200% compared to control, which was partially diminished by MK801. ROS production was measured using fluorescent dye DCF. After 30 min incubation with 75 µg/ml NAg the increase by about 35% over control level was observed and application of MK801 reduced it significantly. Changes in mitochondrial membrane potential were determined using rhodamine (R123). We observed significant decrease in mitochondrial potential during 30 min incubation with different concentrations of NAg and also in this case administration of MK801 was protective. Cells viability was assessed after 24 h incubation with NAg µg/ml alone or together with MK801. Application of MK801 increased neuronal survival from 50% up to 80%. Our results show that excitotoxicity via activation of NMDA receptor, followed by calcium imbalance, destabilization of mitochondrial function and ROS production, seems to be important mechanism involved in neurotoxicity evoked by NAg in cultured neurons. Supported by grant NN401619938.
6

Role of group 1 metabotropic glutamate receptors in homocysteine neurotoxicity

100%
Zieminska E., Stafiej A., Kozlowska H., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
7

Homocysteine neurotoxicity:involvement of calcium and mitochondrial alternations

100%
Zieminska E., Kozlowska H., Stafiej A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
8

Acute cytotoxicity evoked by tetrabromobisphenol A in primary cultures of rat cerebellar granule cells outweighs the effects of polychlorinated biphenyls

100%
Zieminska E., Stafiej A., Toczylowska B., Lazarewicz J. W.
Polish Journal of Environmental Studies
|
2012
|
tom 21
|
nr 4
The aim of this study was to identify, among selected environmental toxins, the substance with the highest in vitro toxicity to neurons combined with the most marked induction of calcium imbalance, oxidative stress and mitochondrial dysfunction. Exposure of primary cultures of rat cerebellar granule cells for 30 min to polychlorinated biphenyls (PCBs) or brominated flame retardants (BFRs) at concentrations of 10-50 µM identified tetrabromobisphenol A as the compound with the highest toxicity. At a concentration of 25 µM, apart from the moderate activation of ⁴⁵Ca uptake, this BFR induced the most pronounced increase in intracellular Ca²⁺ concentration, depolarization of mitochondria, and activation of ROS production.
9
Content available remote

Bastadin 12 and ryanodine reveal similarities between thapsigargin- and tetrabromobisphenol A-induced intracellular Ca2plus release in cultured cerebellar granule cells

100%
Zieminska E., Stafiej A., Toczylowska B., Lazarewicz J. W.
Journal of Physiology and Pharmacology
|
2014
|
tom 65
|
nr 5
10

Modulation of NMDA-evoked prostaglandin D2 release in rabbit hippocampus in vivo

88%
Lazarewicz J. W., Salinska E., Stafiej A., Ziembowicz A., Zieminska E.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
11

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

88%
Lazarewicz J. W., Salinska E., Stafiej A., Ziembowicz A., Zieminska E.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 4
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 Ca concentration ([Ca ]e) and nitric oxide (NO) levels. Samples of dialysate were analysed for changes in PgD2 concentration, in [Ca ]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.
12

Plasma homocysteine level and the course of ischemic stroke

88%
Pniewski J., Chodakowska-Zebrowska M., Wozniak R., Stepien K., Stafiej A.
Acta Neurobiologiae Experimentalis
|
2003
|
tom 63
|
nr 2
13

The role of low molecular weight thiols in thimerosal toxicity - an in votro study

76%
Zieminska E., Toczylowska B., Wojcik J., Stafiej A., Bal W., Lazarewicz J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Thimerosal (TH), an ethylmercury complex of thiosalicylic acid has been used as preservative in vaccines. Inspired by a known high affi nity of mercury for thiol groups, we examined whether the presence of L-cysteine (Cys), D,L-homocysteine (Hcy), Nacetyl cysteine (NAC), L-methionine (Met) and glutathione (GSH) in extracellular space could infl uence the viability, intracellular calcium concentration ([Ca2+]i ) and mitochondrial membrane potential in rat cerebellar granule cells. The cells were exposed to 500 nM TH for 48 h or 15 μM TH for 10 min. The loss of cells viability could be prevented partially or wholly, in a dose-dependent manner, by 60, 120 or 600 μM Cys, Hcy, NAC and GSH, but not by Met. The elevation in [Ca2+]i and mitochondrial potential induced by 25 μM TH were abolished by all compounds studied, except for Met, at 600 μM. The loss of the ethylmercury moiety from TH as a result of interaction with thiols studied was monitored by 1 Hand 199Hg-NMR spectroscopy. This extracelullar process may be responsible for the neuroprotection seen in cerebellar cell culture, but also provides a molecular pathway for redistribution of TH derived toxic ethylmercury in the organism.
14

Neuroprotective potential of methylnicotinamide versus liicotinamide in vivo and in vitro

76%
Slomka M., Makarewicz D., Zieminska E., Duszczyk M., Stafiej A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
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