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1

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

100%
Struzynska L.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
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.
2

Glutathione and glutathione-related enzymes in rat brain after acute lead exposure .

63%
Struzynska L., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
3

The effect of lead on dopamine, GABA and histidine spontaneous and KCI-dependent releases from rat brain synaptosomes

63%
Struzynska L., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
1994
|
tom 54
|
nr 3
4

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

51%
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
5

Astroglia in lead toxicity-neuroprotective or neuro-toxic?

51%
Struzynska L., Sulkowski G., Chalimoniuk M., Lenkiewicz A.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
6

The glial response in the acute lead-induced neurotoxicity in the rat

51%
Struzynska L., Wolski M., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
7

Expression of purinergic P2X(7) receptor in rat brain during the symptomatic phase of experimental autoimmune encephalomyelitis and after recovery of neurological deficits

51%
Grygorowicz T., Sulejczak D., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Purinergic ionotropic P2X7 receptor is widely distributed in brain. Strong evidence suggests that this receptor is related to inflammatory and neurodegenerative changes in many pathological states of central nervous system (CNS), including multiple sclerosis (MS). Experimental autoimmune encephalomyelitis (EAE) is the commonly used animal model of MS. In this study we investigate the expression of P2X7R protein in rat brain in the symptomatic phase of EAE (day 10 post immunization) and after reversion of neurological symptoms (day 20 p.i.). We found the increased level of P2X7R protein in brain homogenates of EAE rats in both examined time windows. Immunohistochemical study revealed enhanced receptor's immunoreactivity. Immunoblots done with isolated cellular brain fractions indicated that the P2X7R overexpression is related to synaptosomal fraction in the symptomatic phase and to the glial (GPV) fraction in the recovery phase of EAE. Concomitantly, we noticed overexpression of astroglial marker GFAP in brain homogenates and astroglial fraction (GPV), so as its enhanced immunoreactivity in brain sections (10 days p.i.) which did not decline to control values in the recovery phase, similarly to P2X7R expression. Results suggest the involvement of P2X7R-mediated signaling in the pathomechanisms of EAE with the possible relevance of astrocytic pool of cells.
8

The role of P2X7R in activation of glial cells during the early phase of experimental autoimmune encephalomyelitis

51%
Grygorowicz T., Welniak-Kaminska M., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Multiple sclerosis (MS) is an autoimmune, neuroinflammatory disease resulting in progressive demyelinization. Glial cells are important players during development of inflammationwithin central nervoussystem.Underinflammatory signals astroglia and microglia change their morphology and up-regulate expression of GFAP and Iba1 proteins, respectively. Both of these cell populations express purinergic receptor P2X7. The aim of the study was to investigate the effect of P2X7R antagonist (Brilliant Blue G, BBG) on the course of experimental autoimmune encephalomyelitis (EAE) with the focus on the influence of BBG-treatment on the reactive gliosis. METHODS: EAE, an animal model of MS, was evoked by the immunization of Lewis rats with guinea pigs’ spinal cord homogenate with complete Freund’s adjuvant. BBG (50 mg/kg) was administered daily from day 0 to day 6 post immunization through the jugular catheter. RESULTS: Immunofluorescent analysis of brain slices showed the activation of astroglial and microglial cells in EAE rats, but not in EAE rats treated with BBG. The expression of GFAP was 5,5 times higher in EAE than in EAE+BBG group at the asymptomatic phase and 3.1 times higher at symptomatic phase of the disease. These results were confirmed by western blot analysis. Expression of Iba1 was 5.4 times and 3.6 times higher in the EAE than in EAE+BBG group at the asymptomatic and symptomatic phases, respectively. The effects of BBG treatment on the expression of proinflammatory cytokines such as IL-1β, IL-6, TNF-α were determined by western blot method. The level of these cytokines was significantly lower in EAE+BBG group than in EAE animals and remained similar to that observed in control rats. CONCLUSIONS: Blockade of P2X7R during the course of EAE results in: (1) improved condition of Animals; (2) decreased activation of astro- and microglia; (3) decreased level of proinflamatory cytokines Supported by Polish National Science Centre, grant nr: DEC-2012- /05/N/NZ4/02191.
9

Influence of DALBK-an antagonist of kinin receptor B1R-on the course of experimental autoimmune encephalomyelitis in rats

51%
Podsiadlo K., Grygorowicz T., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Experimental autoimmune encephalomyelitis (EAE) has been used for several decades as an animal model of multiple sclerosis (MS), an inflammatory demyelinating disease. According to the previous studies mammalian central nervous system presents all components of the kallikrein-kinin system. Biological activity of kinin is mediated by two types of G proteinbound receptors – B1 and B2. Therefore, there are reasons to investigate the participation of B1 receptor in enhancement of the BBB permeability during development of EAE. METHODS: One group of female Lewis rats was immunized by intradermal injection. The second group was injected ip with DALBK (B1R antagonist) after immunization. Control group was not immunized. Rats were monitored daily for clinical signs and loss of weight. Animals were sacrificed in different stages of the disease. Parts of brains were used for Western blotting analysis. Immunohistochemical study was also performed. RESULTS: We noticed the increased level of B1R protein in rat brain in the symptomatic phase of EAE. Animals treated with DALKB exhibited improvement of neurological symptoms and decreased level of B1R protein in most cases. Using a confocal microscope we assessed immunoreactivity of B1R and markers of individual components of glio-vascular unit (astrocytes, endothelial cells and pericytes). We also noticed changes in the level of astroglial markers GFAP and AQP4 during EAE, so as decreased expression of thight jounctions proteins (ZO-1, Occludin, Claudin 5), which were partially abolished by DALBK. CONCLUSIONS: Administration of kinin B1 receptor antagonist (DALBK) significantly improved the condition of animals by reducing the proinflammatory effects of kinins. The results show that the kinin receptor B1 may play a role in pathomechanisms operating during the course of EAE and appears to be a potential therapeutic target. This work was supported by funds from KNOW 2013-2017 project.
10

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

51%
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.
11

The role of astroglia and purinergic signaling in the early stages of EAE

51%
Koza K., Sulkowski G., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
In the CNS an intensive communication between neurons and glial cells occurs. Activation of astrocytes is observed under different pathological conditions, including multiple sclerosis, which results in overexpression of number of proteins, like GFAP and S-100β, which is involved in development of infl ammatory reaction. There is a growing number of evidence that different brain pathologies are characterized by very early active contribution of astrocytes to neurodegenerative axonal damage. Our study presents time-dependent analysis of astroglia-specifi c protein expression in different phases of EAE (from 4 to 25 days after immunization). The biphasic response of astroglia was observed ñ upregulation of both proteins, GFAP and S-100β, in the early stages of the disease and in the peak of the neurological defi cits in animals (10 dpi). Astrocytes build a network within the CNS and are connected by gap junctions, formed by connexins, mostly Cx43 which was shown to induce ATP release via hemichannels. In the cross-talk between astrocytes and neurons may be involved purinergic receptor P2X7, ATP-gated ion channel activated in pathological conditions and participating in regulation of infl ammatory response. In the EAE rats, in the early stages of the disease, we observed the enhanced level of Cx43 protein and P2X7R protein which was accompanied by changes in mRNA profi le. We conclude that early activation of astroglia in the inductive phase of EAE occurs which is connected with the overexpression of purinergic receptor P2X7. The results suggest that in MS/EAE pathology activation of astroglia in the preclinical stage, may contribute to the axonal damage and subsequent infl ammation, and that the purinergic signaling may play a role in both these phenomena.
12

Oxidative stress and inflammatory response in rat brain and live R following oral administration of silver nanoparticles

51%
Skalska J., Frontczak-Baniewicz M., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Silver nanoparticles (AgNPs) are one of the most important class of nanomaterials used in a wide range of medical and industrial applications. However, the information about their toxicity to mammalsislimited. The aim of thisstudy was to investigate the effect of oral exposure to AgNPs on brain and liver of rats. The deposition of silver nanoparticles in these organs has been shown to induce hepatotoxicity and neurotoxicity. These toxic effects may include oxidative stress with subsequent inflammatory response. METHODS: Wistar rats were exposed orally to AgNPs (10±4 nm in diameter) or silver ions at a dose of 0.2 mg AgNPs or Ag+/ kg bw for 14 days. Then all animals were sacrificed 24 h after last exposure and tissues were collected for further studies. RESULTS: The presence of AgNPs in brain tissue was confirmed by using TEM technique. The level of free radicals and end-products of lipid peroxidation increased in both organs after exposure to both, silver nanoparticles or silver ions. However, the changes in inflammatory markers (based on IL-1β, IL-6 and TNF-α relative protein levels) were not statistically significant. CONCLUSIONS: These results show that following AgNPs or silver ions administration, oxidative stress is induced in brain and liver tissues. However, it seems that the time of exposure to both of silver forms was too short to cause the inflammatory response.
13

Cerebral microvessels in rat subjected to EAE: Focus on pericytes and purinergic receptor P2X7

51%
Grygorowicz T., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Blood-brain barrier (BBB) is a structure that maintains central nervous system (CNS) homeostasis by isolating it from the normal blood flow. In physiological conditions BBB prevents CNS penetration by blood-derived molecules and is a barrier for the immune system. BBB is built by tight junctions between endothelial cells of microvessels, pericytes, and astroglial end-feets. Pericytes are very important part of BBB showing a great impact on properties of endothelial cells and BBB tightness. In pathological conditions (i.e. inflammation) the structure of BBB is loosened and cells of the immune system have a free access to the brain and the spinal cord. That is the main mechanism of pathogenesis in both multiple sclerosis (MS) and the rodent model of the disease – experimental autoimmune encephalomyelitis (EAE). Overactivation of purinergic receptor P2X7, is a possible mechanism leading to neurodegeneration observed during the course of MS/EAE. This receptor has two distinct functions: it participates in maturation and release of proinflammatory cytokines or can polymerase to create transmembrane pores which can drive cell to death by apoptosis or necrosis. Thus, we hypothesized that overactivation of this receptor on pericytes may lead to cell damage and/or loss of the protective function towards BBB. In this study we first analyzed status of BBB which was determined by expression of claudin 5 – a marker of BBB tightness – in correlation with the expression of P2X7R in microvessels’ fractions and brain sections of rats subjected to EAE. Using immunoblots and confocal microscopic method we found negative correlation between P2X7R and claudin 5 expression which decreased significantly in all examined time points of the disease, reaching the minimum level (45% and 70% of control) at days 2 p.i. and 4 p.i., respectively. Additionally, we present the results of pericytes features and P2X7R expression in microvessels in early time after EAE induction. Condition of pericytes was visualized by immunofluorescent staining against PDGFRβ (a marker protein). Semiquantitative level of this protein was measured using Western blot analysis of brain homogenates and isolated microvessels fraction. The pattern of observed changes suggests contribution of pericyte-located P2X7R on BBB state and the involvement of this receptor into pathological mechanisms connected with development of EAE.
14

Glial expression of purinergic P2X7 receptor in rat brain during the course of experimental autoimmune encephalomyelitis

51%
Grygorowicz T., Sulejczak D., Sulkowski G., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Multiple sclerosis is a common neurodegenerative disease with prevalence in Poland about 15 per 10000 people. It is characterized by inflamed lesions in myelin sheaths surrounding axons in the white matter of the brain and spinal cord. These changes lead to the damage of axons and, in consequence, to a broad spectrum of neurological symptoms. Experimental autoimmune encephalomyelitis (EAE) is the well known and commonly used animal model of MS. In the present study the temporal pattern of glial activation (microglia and astroglia) together with P2X7R expression were investigated in brain of Lewis rats during the course of EAE. This receptor, activated under pathological conditions, may participate in the regulation of inflammatory response and cell death. It was shown to induce the release of inflammatory mediators like Il-1b and TNF-a in different types of glial cells. It is also pathologically involved in the release of potentially cytotoxic substances like glutamate and ATP. Western blot analysis was used to assess the relative concentration of P2X7R protein in glial fraction whereas its cellular localization was studied by immunohistochemical method. Tissue was labeled with the specific markers (Iba1 - microglial marker, GFAP - astroglial marker) and examined in the different stages post immunization (2, 4, 6, 8, 10 days). We observed the early overexpression of P2X7R protein (2-4 d.p.i.) in glial fraction obtained from brains of EAE rats with parallel enhancement of glial markers. Double immunofluorescent labeling showed colocalization of the receptor with glial markers. The results revealed that activation of both astroglia and microglia takes place very early post immunization, well before the neurological symptoms of the disease occur and is temporary connected with the overexpression of P2X7R. This suggests the involvement of P2X7R-mediated signals into the early pathological mechanisms operating during the disease.
15

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

51%
Struzynska L., Dabrowska-Bouta B., Koza K.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 3
16

Lead and blood-brain barrier in adult rats

51%
Struzynska L., Walski M., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
17

Temporal pattern of glutamate transporters and metabotropic glutamate receptors expression during the course of Experimental Allergic Encephalomyelitis in rats

51%
Sulkowski G., Kwiatkowska-Patzer B., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
18

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

51%
Dabrowska-Bouta B., Struzynska L., Rafalowska U.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
19

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

51%
Koza K., Struzynska L., Dabrowska-Bouta B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
20

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

51%
Podsiadlo K., Dabrowska-Bouta B., Sulkowski G., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2017
|
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.
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