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1

Myelin glycoproteins as a target of Ph in the rodent model of prolonged exposure

100%
Dabrowska-Bouta B., Walski M., Rafalowska U.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
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nr 4
2

Modulation of neurological deficits during EAE by glutamate receptors antagonists MPEP and amantadine

100%
Sulkowski G., Dabrowska-Bouta B., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Chronic glutamate-mediated excitotoxicity has been suggested to contribute to the pathogenesis of Multiple Sclerosis (MS). Recent data suggest that inhibition of glutamate neurotransmission via specific interaction with glutamate receptors (GluRs) might be interesting for inhibition of disease progression and early symptomatic treatment in MS. The aim of our investigation was to study the role of NMDA receptors and group I mGluRs in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. We tested the effect of MPEP (2-methyl-6-(phenylethynyl)-pyridine), the mGluR5 antagonist, in dose of 5 mg/kg b.w./day, and amantadine (the uncompetitive NMDA receptor antagonist) in dose of 100 mg/kg b.w./day on development of neurological deficits in EAE rats. Both drugs were administered intraperitoneally ones daily into EAE rats during 7 days, starting from day 5 to 12 post immunization. The neurological symptoms of EAE started at 10-11 days post immunization and peaked after 12-13 days. We noted the changes in body weight during the course of EAE. Until day 8 p.i. the body weight of rats in control and treated groups was in the same range. Starting from day 8 p.i. rats in all groups showed a progressive weight loss by about 20-30% until day 14 p.i. Application of amantadine was found to be effective and significantly reduced neurological symptoms of EAE. We did not observed any neuroprotective effects of MPEP. The level of mGluR5 protein did not increase in early phase of EAE (4 day p.i.). However, starting from day 8 p.i. to day 25 p.i. we observed its significant elevation. The difference between control and examined group reached 20% at 25 day p.i. We did not observe significant differences in mGluR5 level between three experimental groups: EAE rats (control), MPEP-treated and amantadine-treated rats. Our results confirm the involvement of glutamate into pathogenesis of EAE. Although we noted changes in the expression of mGluR 5 during the course of EAE, MPEP was ineffective in reducing the symptoms of the disease. Results suggest the main role of NMDA glutamate receptors in the pathogenesis of EAE. Research was supported by funds from grant nr: NN401620038 from Polish Ministry of Scientific and Higher Education
3

Response of glia in hippocampus of immature rat brain after prolonged Pb exposure

100%
Struzynska L., Dabrowska-Bouta B., Koza K.
Acta Neurobiologiae Experimentalis
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2007
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tom 67
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nr 3
4

Changes in the level of -SH groups in brain under lead-toxicity conditions

100%
Dabrowska-Bouta B., Struzynska L., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
1995
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tom 55
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nr 5
5

Inflammatory features of glial reaction in immature lead-exposed rat brain

100%
Koza K., Struzynska L., Dabrowska-Bouta B.
Acta Neurobiologiae Experimentalis
|
2006
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tom 66
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nr 4
6

Possible involvement of kinin B1 receptor in the development of experimental autoimmune encephalomyelitis in rats

100%
Podsiadlo K., Dabrowska-Bouta B., Sulkowski G., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2017
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tom 77
|
nr Suppl.1
INTRODUCTION: Experimental autoimmune encephalomyelitis (EAE) is the most commonly used animal model of multiple sclerosis (MS) which is neuroinflammatory demyelinating disease of autoimmune origin. Among inflammatory mediators, kinins are bioactive peptides critically involved in regulation of the inflammatory response and vascular permeability. These biological activities of kinins are mediated by B1 receptors through the release of pro-inflammatory cytokines. AIM(S): Therefore, there are reasons to investigate the role of B1 receptor in the enhancement of the BBB permeability during development of EAE. METHOD(S): Group of female Lewis rats was immunized by intradermal injection of 100 μl inoculum. The second group was injected i.p. with DALBK (B1R antagonist) after immunization. Control group was not immunized. Animals were sacrificed in different stages of the disease. Parts of brains were used for Western blotting analysis and measurement of inflammatory cytokines using RayBio Rat Cytokine Antibody Array (RayBiotech, Inc.). Immunohistochemical study on isolated fraction of microvessels was also performed. Gene expression was quantified by RT-PCR RESULTS: We noticed the increased expression of B1R in rat brain and isolated fraction of microvessels in the symptomatic phase of EAE. Animals treated with DALBK exhibited improvement of neurological symptoms and decreased overexpression of B1R. We also noticed increased protein level of chemokines and proinflammatory cytokines. Using a confocal microscope, we observed lowered immunoreactivity of thight junctions proteins (ZO-1, occludin, claudin 5) and pericytes markers (PDGFβR and angiopoietin‑1) in microvessels’ fraction obtained from EAE rats which increased after DALBK. CONCLUSIONS: Administration of kinin B1 receptor antagonist (DALBK) significantly improved the condition of animals. Results show that B1R‑mediated pro‑inflammatory effect of kinins may be involved in pathomechanisms operating during EAE which may lead to enhanced permeability of microvessels.
7

Acute lead toxicity and energy metabolism in rat brain synaptosomes

100%
Struzynska L., Dabrowska-Bouta B., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 4
8

Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes ?

100%
Rafalowska U., Struzynska L., Dabrowska-Bouta B., Lenkiewicz A.
Acta Neurobiologiae Experimentalis
|
1996
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tom 56
|
nr 2
9

Effect of acute and chronic lead exposure on the level of sulfhydryl groups in rat brain

100%
Dabrowska-Bouta B., Struzynska L., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
1996
|
tom 56
|
nr 1
10

Glutamate receptors antagonists attenuate neurological deficits and modulate neuroinflammation in Lewis rat subjected to experimental autoimmune encephalomyelitis

88%
Sulkowski G., Dabrowska-Bouta B., Chalimoniuk M., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Experimental autoimmune encephalomyelitis (EAE) is an animal model that mimics many aspects of multiple sclerosis (MS). Chronic or relapsing inflammation of the central nervous system results in the destruction of myelin sheath and cytokines play an important role in the pathogenesis of both MS and EAE. Myelin, oligodendrocytes and neurons are lost due to an inflammatory attack by leukocytes infiltrating the central nervous system (CNS) and releasing cytotoxic cytokines, anti CNS antibodies and large amounts of the excitatory neurotransmitter glutamate. Pharmacological studies have suggested that glutamate receptors mediate white matter injury in a variety of CNS diseases, including multiple sclerosis (MS). Memantine and amantadine are ionotropic glutamate receptors (iGluRs) antagonists. Memantine, a clinically applied drug with N-methyl-D-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rats subjected to experimental autoimmune encephalomyelitis (EAE). The aim of the present study was to investigate the effects of memantine and amantadine on the expression of proinflammatory cytokines such interleukin 1beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and various chemokines in the brain of EAE rats. Real-time Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western Blot were used to analyze the cytokine profile. We noticed increased expression of array of cytokines in experimental group when compared to the control. Dramatic increase of IL-1β, IL-6, TNF-α, and chemokines concentration corresponding to the intensity of neurological symptoms and loss of weight was observed in EAE rats. Administration of iGluR antagonists at an advanced stage of unremitting EAE resulted in amelioration of the disease. Cytokine analysis revealed that memantine significantly decreased the expression of interleukins: IL-6 (65%), IL-1β (60%) and TNF-α (45%) whereas treatment with amantadine reduced only the expression of IL-6 (60%) and TNF-α (15%) when compared to EAE animals. These results show that antagonists of iGlu receptors modulate the course of the disease by reducing the expression of proinflammatory cytokines thereby confirming the involvement of glutamate receptors into pathological mechanisms operating during EAE. This study was supported by grant nr NN401620038 from Polish Ministry of Science and Higher Education
11

Glutamate excitotoxicity in pathogenesis of multiple sclerosis

88%
Sulkowski G., Struzynska L., Dabrowska-Bouta B., Kwiatkowska-Pozer B., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
12

The effect of a sphingosine-1-phosphate receptors modulator on the transcriptional profile of genes linked to glutamate homeostasis in the sporadic and genetic animal models of Alzheimer’s disease

88%
Wencel P., Sulkowski G., Dabrowska-Bouta B., Strosznajder R. P., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: Alzheimer’s disease (AD) is neurodegenerative disorder characterized by progressive memory impairment and cognitive failure which leads to dementia in aged population. Lots of data indicate glutamate-mediated neurotoxicity as a one of the pathomechanisms responsible for neuronal cell death during the course of AD. AIM(S): In this study, we examined the effect of fingolimod (FTY720‑modulator of sphingosine‑1‑phosphate receptors) on the transcription of genes involved in the homeostasis of glutamatergic system in animal models of AD. METHOD(S): 3‑ and 12‑month‑old (3M, 12M) FVB/ APP+ transgenic mice with the London (V717I) APP mutation were used in this study. Mice without the mutation (APP- ) were used as a control. The sporadic AD model was induced by injection of streptozotocin (STZ, icv. 2,5 mg/kg b.w.) in ACSF (vehicle) to 3M C57BL/6 mice. Animals received FTY720 (1mg/kg b.w.) or NaCl (vehicle) for 2 weeks. Brain cortex was isolated and qPCR methods were applied. RESULTS: Our results indicate a different model‑dependent profile of changes in gene expression. We observed significant upregulation of Slc17a7(VGluT1), Grin1(- GluN1), and Grm3 (mGluR3) gene expression in APP+ 12M mice. A significant elevation of Gria1(GluR‑1) and Grin1 (GluN1) mRNA levels with an accompanying decrease of Slc17a8 (VGluT3) and Grm5 (mGluR5) was observed in STZ mice. The administration of FTY720 led to a decrease in Gria2 (GluR-2) and Grm3 mRNA levels, as well as, an elevation of Slc1a3 (GluT‑1), Slc17a7, and Slc17a8 mRNA in STZ mice compared to appropriate controls. Transcriptional changes in vesicular glutamate transporters (Slc17a7 and Slc17a8) as well as glutamate receptors genes (Grin1, Gria1, Grm3,5) suggest that they may be involved in the mechanisms leading to AD. CONCLUSIONS: FTY720 may potentially modulate the expression of genes involved in homeostasis of the glutamatergic system in the model of sporadic AD. FINANCIAL SUPPORT: Supported by the National Science Centre grant no. NCN2014/15/B/NZ3/01049
13

Glutamate transporters in rat brain exposed to polychlorinated biphenyls and polibrominated flame retardants

88%
Sulkowski G., Struzynska L., Dabrowska-Bouta B., Albrecht J., Lazarewicz J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Polychlorinated biphenyl (PCB) congeners and polibrominated fl ame retardants (BFRs) are environmentally occurring toxins that exhibit a broad range of adverse biological effects including neurotoxicity. Due to their stability and lipophilic character, they persist in the environment and accumulate in brain of animals and humans contributing to induction of neurological disorders. The mechanisms by which PCBs and BFRs cause neurotoxic effects are still not completely understood. However, it is postulated that glutamate excitotoxicity may be involved. The main glutamate transporters GLT-1 and GLAST are membrane-bound proteins localized in glial cells. The clearance of synaptically released glutamate by these proteins protects neurons from excitotoxicity. The aim of the study was to establish whether the chronic exposure to these substances may infl uence the expression and activity of main glutamate transporters in rat brain. Aroclor 1254 (PCBs) and tetrabromobisphenol A (BFRs) were administered by oral gavage, which resembles the human exposure through the food chain, for two weeks. Signifi cant changes in the expression of glutamate transporters were observed, especially in the case of GLT-1. The effect was more pronounced for Aroclor 1254. The results suggest that GLT-1 is a molecular target of this toxin that may, almost partially, contribute to PCBs-induced excitotoxicity. This study was supported by grant nr NN401024635 from Polish Ministry of Science and Higher Education.
14

The influence of silver nanoparticles on blood-brain barrier function and morphology in adult rats

88%
Sulkowski G., Dabrowska-Bouta B., Orzelska-Gorka J., Frontczak-Baniewicz M., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Neurotoxicity of silver nanoparticles has been confirmed in a lot of in vitro and in vivo studies using different experimental models. However, the mechanisms of the toxic action have not been fully clarified. Since nanoparticles have the ability to enter the brain and significantly accumulate in this organ, it is important to investigate their neurotoxic mechanisms. AIM(S): We examined the effect of prolonged exposure on blood-brain barrier (BBB) ultrastructure and expression of tight junctions protein components as opposed to the ionic silver. METHOD(S): In the current study we exposed adult rats to a low dose (0.2 mg/kg b.w.) of small (10 nm) citrate-stabilized silver nanoparticles (AgNPs). RESULTS: The BBB is a highly specialized structure composed of a basement membrane and microvascular endothelial cells which interact with pericytes, perivascular artrocytes and neurons forming neurovascular unit. Administration of AgNPs over a two-week period resulted in changes in BBB ultrastructure and integrity. TEM analysis revealed accumulation of AgNPs inside endothelial cells of microvessels, mainly in lysosomes. Ultrastructural features of enhanced permeability of cerebral microvessels were observed such as enhanced activity of pinocytotic vesicular system and swollen perivascular astrocytic end-feets. This suggests uptake of fluid and its transfer to parenchyma which further results in perivascular edema. Additionally, we observed changes in the level of mRNA of the main tight junction proteins such as claudine, ocludine, and ZO1 as well as PDGF and its receptor PDGFbR which constitute the signaling pathway between endothelial cells and pericytes. All these characteristic protein components are responsible for the integrity of BBB. CONCLUSIONS: The results of the current study demonstrate that exposure of adult rats to AgNPs induces BBB dysfunction leading to the enhanced permeability of cerebral microvessels.
15

Some metabolic effects in rat brain synaptosomes after exposure to lead in vivo and in vitro

88%
Struzynska L., Dabrowska-Bouta B., Lenart J., Zborowski J., Rafalowska U.
Bulletin of the Polish Academy of Sciences. Biological Sciences
|
1994
|
tom 42
|
nr 1
16

Ultrastructural and biochemical changes in brain of rat chronically exposed to silver nanoparticles

76%
Widynska J., Dabrowska-Bouta B., Frontczak-Baniewicz M., Lenkiewicz A., Grygorowicz T., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Silver nanoparticles (AgNPs) demonstrate strong antimicrobial activity resulting in their wide-spread use in different applications, including medical ones. Despite of the fact that human exposure to nanosilver is constantly increasing, there is no many research dedicated for investigating their potential neurotoxic effects. Most of the previous studies on mechanisms of nanosilver neurotoxicity have used in vitro models. The aim of the present study was to determine whether this small-sized commercially available AgNPs induce ultrastructural and biochemical changes in brain of male adult rats. Rats were exposed orally to 10 ± 4 nm nanosilver in size for 14 days. Using transmission electron microscopy (TEM), nanosized granules were detected in brains of exposed rats. Besides, ultrastructural changes in cortical and hippocampal neurons were found. TBARs level was measured to assessed lipid peroxidation in homogenates from exposed animals and immunochemical analysis was used to measure the level of selected tissue markers of oxidative stress in brain. Supported by grant nr NN401619938.
17

Effects of IFN-beta1a and IFN-beta1b treatment on the expression of cytokines, inducible NOS (NOS type II), and myelin proteins in animal model of multiple sclerosis

76%
Lubina-Dabrowska N., Stepien A., Sulkowski G., Dabrowska-Bouta B., Langfort J., Chalimoniuk M.
Archivum Immunologiae et Therapiae Experimentalis
|
2017
|
tom 65
|
nr 4
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