TY  - JOUR
AU  - Dacić, Sanja
AU  - Božić, Iva
AU  - Jeremić, Rada
AU  - Bjelobaba, Ivana
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
AU  - Peković, Sanja
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5989
AB  - Aims: Traumatic brain injury (TBI) causes disruption in homeostasis of calcium ions (Ca2+), important second messenger considered as the major culprit of secondary injury and TBI-induced neuronal damage and death. Ca2+ entry into the cells occurs via various types of voltage-dependent calcium channels (VDCCs). The aim of this study was to evaluate the involvement of Ca2+ entry via L-type CaV1.2 VDCCs in the processes of neuroinflammation and regeneration after brain injury. Methods: TBI was performed on male Wistar rats by sensorimotor cortex ablation (SCA) at the following coordinates: 2 mm anterior and 4 mm posterior to bregma, and 4 mm lateral from the midline. Temporal and cellular pattern of CaV1.2 expression was followed at different time points post-injury (2, 7, 14, 30 dpi) using double immunofluorescence staining with specific markers. Results: Upregulation of CaV1.2 expression was detected on reactive astrocytes and astrocytic processes that form glial scar around the lesion site, on subset of proinflammatory microglia/macrophages and neutrophils surrounding the lesion cavity. Interestingly, presence of CaV1.2+ cells was detected in the migratory pathway, consisted of DCX+ progenitors, extending from subventricular zone up to the lesion site. Furthermore, CaV1.2+/DCX+ newborn neurons were detected in subgranular layer of hippocampal dentate gyrus. Conclusions: We concluded that L-type CaV1.2 calcium channel has an important role in the regulation of processes of neuroinflammation, neuroregeneration and neurogenesis, pointing to the complexity of intercellular regulation of Ca2+ homeostasis after brain injury. Consequently, modulation of CaV1.2 channels expression may be potential target for the treatment of brain injury.
PB  - Belgrade: Serbian Neuroscience Society
T2  - Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
T1  - L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury
SP  - 487
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5989
ER  - 

@article{
author = "Dacić, Sanja and Božić, Iva and Jeremić, Rada and Bjelobaba, Ivana and Lavrnja, Irena and Savić, Danijela and Rakić, Ljubisav and Stojiljković, Mirjana and Peković, Sanja",
year = "2019",
abstract = "Aims: Traumatic brain injury (TBI) causes disruption in homeostasis of calcium ions (Ca2+), important second messenger considered as the major culprit of secondary injury and TBI-induced neuronal damage and death. Ca2+ entry into the cells occurs via various types of voltage-dependent calcium channels (VDCCs). The aim of this study was to evaluate the involvement of Ca2+ entry via L-type CaV1.2 VDCCs in the processes of neuroinflammation and regeneration after brain injury. Methods: TBI was performed on male Wistar rats by sensorimotor cortex ablation (SCA) at the following coordinates: 2 mm anterior and 4 mm posterior to bregma, and 4 mm lateral from the midline. Temporal and cellular pattern of CaV1.2 expression was followed at different time points post-injury (2, 7, 14, 30 dpi) using double immunofluorescence staining with specific markers. Results: Upregulation of CaV1.2 expression was detected on reactive astrocytes and astrocytic processes that form glial scar around the lesion site, on subset of proinflammatory microglia/macrophages and neutrophils surrounding the lesion cavity. Interestingly, presence of CaV1.2+ cells was detected in the migratory pathway, consisted of DCX+ progenitors, extending from subventricular zone up to the lesion site. Furthermore, CaV1.2+/DCX+ newborn neurons were detected in subgranular layer of hippocampal dentate gyrus. Conclusions: We concluded that L-type CaV1.2 calcium channel has an important role in the regulation of processes of neuroinflammation, neuroregeneration and neurogenesis, pointing to the complexity of intercellular regulation of Ca2+ homeostasis after brain injury. Consequently, modulation of CaV1.2 channels expression may be potential target for the treatment of brain injury.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia",
title = "L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury",
pages = "487",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5989"
}

Dacić, S., Božić, I., Jeremić, R., Bjelobaba, I., Lavrnja, I., Savić, D., Rakić, L., Stojiljković, M.,& Peković, S.. (2019). L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 487.
https://hdl.handle.net/21.15107/rcub_ibiss_5989

Dacić S, Božić I, Jeremić R, Bjelobaba I, Lavrnja I, Savić D, Rakić L, Stojiljković M, Peković S. L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia. 2019;:487.
https://hdl.handle.net/21.15107/rcub_ibiss_5989 .

Dacić, Sanja, Božić, Iva, Jeremić, Rada, Bjelobaba, Ivana, Lavrnja, Irena, Savić, Danijela, Rakić, Ljubisav, Stojiljković, Mirjana, Peković, Sanja, "L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury" in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia (2019):487,
https://hdl.handle.net/21.15107/rcub_ibiss_5989 .

TY  - JOUR
AU  - Savić, Danijela
AU  - Stanković, Tijana
AU  - Lavrnja, Irena
AU  - Podolski-Renić, Ana
AU  - Banković, Jasna
AU  - Peković, Sanja
AU  - Stojiljković, Mirjana
AU  - Rakić, Ljubisav
AU  - Ruždijić, Sabera
AU  - Pešić, Milica
PY  - 2015
UR  - http://www.degruyter.com/view/j/motth.2015.1.issue-1/motth-2015-0002/motth-2015-0002.xml
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2633
AB  - Purine nucleoside analogs have been in clinical use for almost 50 years. At the beginning developed as antiviral agents, later their efficacy was demonstrated in cancer treatment, especially hematological malignances. The approval of new purine nucleoside analogs by US Food and Drug Administration (FDA) over the past decade implies that the interest for these drugs still exists. Here, we review new nucleoside analogs that are currently in preclinical or clinical development as anticancer agents. In addition, we highlight the potential for implementation of these drugs in other pathological conditions, particularly in neuroinflammation.
T2  - Molecular inhibitors in targeted therapy
T1  - Purine nucleoside analogs in the therapy of cancer and neuroinflammation
IS  - 1
VL  - 1
DO  - 10.1515/motth-2015-0002
SP  - 3
EP  - 14
ER  - 

@article{
author = "Savić, Danijela and Stanković, Tijana and Lavrnja, Irena and Podolski-Renić, Ana and Banković, Jasna and Peković, Sanja and Stojiljković, Mirjana and Rakić, Ljubisav and Ruždijić, Sabera and Pešić, Milica",
year = "2015",
abstract = "Purine nucleoside analogs have been in clinical use for almost 50 years. At the beginning developed as antiviral agents, later their efficacy was demonstrated in cancer treatment, especially hematological malignances. The approval of new purine nucleoside analogs by US Food and Drug Administration (FDA) over the past decade implies that the interest for these drugs still exists. Here, we review new nucleoside analogs that are currently in preclinical or clinical development as anticancer agents. In addition, we highlight the potential for implementation of these drugs in other pathological conditions, particularly in neuroinflammation.",
journal = "Molecular inhibitors in targeted therapy",
title = "Purine nucleoside analogs in the therapy of cancer and neuroinflammation",
number = "1",
volume = "1",
doi = "10.1515/motth-2015-0002",
pages = "3-14"
}

Savić, D., Stanković, T., Lavrnja, I., Podolski-Renić, A., Banković, J., Peković, S., Stojiljković, M., Rakić, L., Ruždijić, S.,& Pešić, M.. (2015). Purine nucleoside analogs in the therapy of cancer and neuroinflammation. in Molecular inhibitors in targeted therapy, 1(1), 3-14.
https://doi.org/10.1515/motth-2015-0002

Savić D, Stanković T, Lavrnja I, Podolski-Renić A, Banković J, Peković S, Stojiljković M, Rakić L, Ruždijić S, Pešić M. Purine nucleoside analogs in the therapy of cancer and neuroinflammation. in Molecular inhibitors in targeted therapy. 2015;1(1):3-14.
doi:10.1515/motth-2015-0002 .

Savić, Danijela, Stanković, Tijana, Lavrnja, Irena, Podolski-Renić, Ana, Banković, Jasna, Peković, Sanja, Stojiljković, Mirjana, Rakić, Ljubisav, Ruždijić, Sabera, Pešić, Milica, "Purine nucleoside analogs in the therapy of cancer and neuroinflammation" in Molecular inhibitors in targeted therapy, 1, no. 1 (2015):3-14,
https://doi.org/10.1515/motth-2015-0002 . .

TY  - JOUR
AU  - Parabucki, Ana
AU  - Savić, Danijela
AU  - Laketa, Danijela
AU  - Peković, Sanja
AU  - Stojiljković, Mirjana
AU  - Nedeljković, Nadežda
AU  - Bjelobaba, Ivana
PY  - 2014
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5864
AB  - Ectonucleotidases are cell surface-located enzymes responsible for the extracellular degradation of nucleotides. They are comprised of several protein families: ectonucleoside triphosphate diphosphohydrolases (E-NTPDase), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPases) and ecto-5'-nucleotidase. Previously we showed that cortical stab injury alters ectonucleotidase activities in the rat brain, but that the specific enzymes responsible for these changes were not identified. In this study we investigated the gene expression of the specific ectonucleotidase enzymes, NTP-Dase1-3, NPP1-3 and ecto-5'-nucleotidase, two and seven days after cortical stab injury in rats, using real-time PCR. Two days after the injury we observed only one significant change: the downregulation in NTPDase2 mRNA expression. Our results indicate that traumatic brain injury induces significant upregulation of NTPDasel, NTPDase2 and ecto-5'-nucleotidase transcripts, and the downregulation of NPP1, seven days after the injury. Thus, traumatic brain injury has diverse impacts on ectonucleotidases gene expression, which may be reflected in the enzyme activities and extracellular nucleotide concentrations in the perilesional tissue.
PB  - Belgrade: Serbian Biological Society
T2  - Archives of Biological Sciences
T1  - Expression of major ectonucleotidases after cortical stab brain injury in rats: A real-time PCR study
IS  - 1
VL  - 66
DO  - 10.2298/ABS1401148P
SP  - 149
EP  - 155
ER  - 

@article{
author = "Parabucki, Ana and Savić, Danijela and Laketa, Danijela and Peković, Sanja and Stojiljković, Mirjana and Nedeljković, Nadežda and Bjelobaba, Ivana",
year = "2014",
abstract = "Ectonucleotidases are cell surface-located enzymes responsible for the extracellular degradation of nucleotides. They are comprised of several protein families: ectonucleoside triphosphate diphosphohydrolases (E-NTPDase), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPases) and ecto-5'-nucleotidase. Previously we showed that cortical stab injury alters ectonucleotidase activities in the rat brain, but that the specific enzymes responsible for these changes were not identified. In this study we investigated the gene expression of the specific ectonucleotidase enzymes, NTP-Dase1-3, NPP1-3 and ecto-5'-nucleotidase, two and seven days after cortical stab injury in rats, using real-time PCR. Two days after the injury we observed only one significant change: the downregulation in NTPDase2 mRNA expression. Our results indicate that traumatic brain injury induces significant upregulation of NTPDasel, NTPDase2 and ecto-5'-nucleotidase transcripts, and the downregulation of NPP1, seven days after the injury. Thus, traumatic brain injury has diverse impacts on ectonucleotidases gene expression, which may be reflected in the enzyme activities and extracellular nucleotide concentrations in the perilesional tissue.",
publisher = "Belgrade: Serbian Biological Society",
journal = "Archives of Biological Sciences",
title = "Expression of major ectonucleotidases after cortical stab brain injury in rats: A real-time PCR study",
number = "1",
volume = "66",
doi = "10.2298/ABS1401148P",
pages = "149-155"
}

Parabucki, A., Savić, D., Laketa, D., Peković, S., Stojiljković, M., Nedeljković, N.,& Bjelobaba, I.. (2014). Expression of major ectonucleotidases after cortical stab brain injury in rats: A real-time PCR study. in Archives of Biological Sciences
Belgrade: Serbian Biological Society., 66(1), 149-155.
https://doi.org/10.2298/ABS1401148P

Parabucki A, Savić D, Laketa D, Peković S, Stojiljković M, Nedeljković N, Bjelobaba I. Expression of major ectonucleotidases after cortical stab brain injury in rats: A real-time PCR study. in Archives of Biological Sciences. 2014;66(1):149-155.
doi:10.2298/ABS1401148P .

Parabucki, Ana, Savić, Danijela, Laketa, Danijela, Peković, Sanja, Stojiljković, Mirjana, Nedeljković, Nadežda, Bjelobaba, Ivana, "Expression of major ectonucleotidases after cortical stab brain injury in rats: A real-time PCR study" in Archives of Biological Sciences, 66, no. 1 (2014):149-155,
https://doi.org/10.2298/ABS1401148P . .

TY  - JOUR
AU  - Laketa, Danijela
AU  - Bjelobaba, Ivana
AU  - Savić, Danijela
AU  - Lavrnja, Irena
AU  - Parabucki, Ana
AU  - Stojiljković, Mirjana
AU  - Nedeljković, Nadežda
PY  - 2013
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/326
AB  - Injury and other pathological conditions induce a massive release of ATP and ADP that initiate an immune response. Extracellular nucleotides are degraded by ectonucleotidases: enzymes from E-NTPDase and E-NPP families sequentially hydrolyze ATP and ADP to AMP, which is further hydrolyzed by ecto-5'-nucleotidase to adenosine that exerts suppressive effects on immune cells. We investigated the ectonucleotidase activities of peripheral lymphocytes at different post-injury times after an unilateral brain injury in the rat. Significant and dynamic changes in the lymphocytic ectonucleotidase activities were obtained. ATP- and ADP-hydrolysis changes, together with their calculated ratios, indicate the major contribution of E-NTPDase 1 and its comparable upregulation between sham operation and injury. AMP hydrolysis changes were more brain-injury specific, with a longer-lasting lymphocytic response induced by cortical stab injury (CSI). In summary, CSI and sham operation induce the upregulation of the whole enzyme chain for adenine nucleotide hydrolysis in lymphocytes, suggesting an important roles of ectonucleotidases in the course of recovery after brain injury.
T2  - Archives of Biological Sciences
T1  - Brain cortical injury induces changes in peripheral lymphocyte ectonucleotidase activities
IS  - 1
VL  - 65
SP  - 33
EP  - 42
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_326
ER  - 

@article{
author = "Laketa, Danijela and Bjelobaba, Ivana and Savić, Danijela and Lavrnja, Irena and Parabucki, Ana and Stojiljković, Mirjana and Nedeljković, Nadežda",
year = "2013, 2013",
abstract = "Injury and other pathological conditions induce a massive release of ATP and ADP that initiate an immune response. Extracellular nucleotides are degraded by ectonucleotidases: enzymes from E-NTPDase and E-NPP families sequentially hydrolyze ATP and ADP to AMP, which is further hydrolyzed by ecto-5'-nucleotidase to adenosine that exerts suppressive effects on immune cells. We investigated the ectonucleotidase activities of peripheral lymphocytes at different post-injury times after an unilateral brain injury in the rat. Significant and dynamic changes in the lymphocytic ectonucleotidase activities were obtained. ATP- and ADP-hydrolysis changes, together with their calculated ratios, indicate the major contribution of E-NTPDase 1 and its comparable upregulation between sham operation and injury. AMP hydrolysis changes were more brain-injury specific, with a longer-lasting lymphocytic response induced by cortical stab injury (CSI). In summary, CSI and sham operation induce the upregulation of the whole enzyme chain for adenine nucleotide hydrolysis in lymphocytes, suggesting an important roles of ectonucleotidases in the course of recovery after brain injury.",
journal = "Archives of Biological Sciences",
title = "Brain cortical injury induces changes in peripheral lymphocyte ectonucleotidase activities",
number = "1",
volume = "65",
pages = "33-42",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_326"
}

Laketa, D., Bjelobaba, I., Savić, D., Lavrnja, I., Parabucki, A., Stojiljković, M.,& Nedeljković, N.. (2013). Brain cortical injury induces changes in peripheral lymphocyte ectonucleotidase activities. in Archives of Biological Sciences, 65(1), 33-42.
https://hdl.handle.net/21.15107/rcub_ibiss_326

Laketa D, Bjelobaba I, Savić D, Lavrnja I, Parabucki A, Stojiljković M, Nedeljković N. Brain cortical injury induces changes in peripheral lymphocyte ectonucleotidase activities. in Archives of Biological Sciences. 2013;65(1):33-42.
https://hdl.handle.net/21.15107/rcub_ibiss_326 .

Laketa, Danijela, Bjelobaba, Ivana, Savić, Danijela, Lavrnja, Irena, Parabucki, Ana, Stojiljković, Mirjana, Nedeljković, Nadežda, "Brain cortical injury induces changes in peripheral lymphocyte ectonucleotidase activities" in Archives of Biological Sciences, 65, no. 1 (2013):33-42,
https://hdl.handle.net/21.15107/rcub_ibiss_326 .

TY  - JOUR
AU  - Savić, Danijela
AU  - Parabucki, Ana
AU  - Bjelobaba, Ivana
AU  - Santrač, Anja
AU  - Dacić, Sanja
AU  - Peković, Sanja
AU  - Stojiljković, Mirjana
PY  - 2013
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/507
AB  - Background: Various in vivo and in vitro models have been described in order to elucidate the pathobiology underlying the traumatic brain injury (TBI) and test potentially suitable treatments. Since TBI is a complex disease, models differ in regard to the aspect of TBI that is being investigated. One of the used in vitro models is the scratch wound assay, first established as a reproducible, low-cost assay for the analysis of cell migration in vitro. The aim of the present study was to further investigate the relevancy of this model as a counter­part of in vivo TBI models. Methods: We have examined the astrocytic response to a mechanical injury in terms of expression of chondroitin sulfate proteoglycans (CSPGs) - phosphacan, neurocan and brevican, using real-time PCR and immunocytochemistry. Results: Our results indicate that in vitro scratch wounding alters the expression profile of examined CSPGs. Four hours after the scratch injury of the astrocytic monolayer, real-time PCR analysis revealed upregulation of mRNA levels for phosphacan (3-fold) and neurocan (2-fold), whereas brevican mRNA was downregulated (2-fold). Immunofluorescent signal for phosphacan and neurocan was more intense in astrocytes close to the injury site, while brevican was scarcely present in cultured astrocytes. Conclusions: Obtained results indicate that CSPGs are differentially expressed by astrocytes after scratch wounding, demonstrating that the scratch wound model might be suitable for investigation of astrocyte-derived response to injury.
AB  - Uvod: Brojni in vivo i in vitro modeli opisani su sa ciljem da se rasvetle patobiološki procesi koji su osnova traumatske povrede mozga (TPM) i testiraju potencijalni tretmani. Imajući u vidu da je TPM kompleksno oboljenje, ovi modeli se međusobno razlikuju shodno aspektu TPM koji se ispituje. Jedan od in vitro modela je i povreda ćelijskog jednosloja grebanjem (engl. 'scratch wound' assay), isprva ustanovljen kao ponovljiv, jeftin test za analizu celijske migracije in vitro. Cilj ove studije je da se bliže ispita relevantnost ovog modela u odnosu na in vivo modele TPM. Metode: Da bi se istražio odgovor astrocita na mehaničku povredu, praćena je ekspresija odabranih hondroitin-sulfatnih proteoglikana (CSPG) - fosfakana, neurokana i brevikana, korišćenjem PCR u realnom vremenu i imunocitohemije. Rezultati: Dobijeni rezultati su pokazali da in vitro povreda astrocitnog jednosloja menja profile ekspresije ispitivanih CSPG. Četiri sata nakon povrede, primena PCR u realnom vremenu analize pokazala je povećanje nivoa iRNK za fosfakan (trostruko) i neurokan (dvostruko), dok je iRNK za brevikan bila smanjena na polovinu kontrolne vrednosti. Imunofluorescentni signal poreklom od fosfakana i neurokana je bio intenzivniji u astrocitima bližim mestu povrede, dok je signal za brevikan bio slab kako u kontrolnoj, tako i u ozleđenoj grupi. Zaključak: Dobijeni rezultati pokazuju da povreda izazvana grebanjem različito utiče na ekspresiju ispitivanih CSPG u astrocitima, sto ukazuju da ovaj model može biti pogodan za ispitivanje odgovora astrocita na povredu.
T2  - Journal of Medical Biochemistry
T1  - PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi
T1  - Real-time PCR and immunocytochemical study of chondroitin sulfate proteoglycans after scratch wounding in cultured astrocytes
IS  - 4
VL  - 32
SP  - 398
EP  - 405
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_507
ER  - 

@article{
author = "Savić, Danijela and Parabucki, Ana and Bjelobaba, Ivana and Santrač, Anja and Dacić, Sanja and Peković, Sanja and Stojiljković, Mirjana",
year = "2013, 2013",
abstract = "Background: Various in vivo and in vitro models have been described in order to elucidate the pathobiology underlying the traumatic brain injury (TBI) and test potentially suitable treatments. Since TBI is a complex disease, models differ in regard to the aspect of TBI that is being investigated. One of the used in vitro models is the scratch wound assay, first established as a reproducible, low-cost assay for the analysis of cell migration in vitro. The aim of the present study was to further investigate the relevancy of this model as a counter­part of in vivo TBI models. Methods: We have examined the astrocytic response to a mechanical injury in terms of expression of chondroitin sulfate proteoglycans (CSPGs) - phosphacan, neurocan and brevican, using real-time PCR and immunocytochemistry. Results: Our results indicate that in vitro scratch wounding alters the expression profile of examined CSPGs. Four hours after the scratch injury of the astrocytic monolayer, real-time PCR analysis revealed upregulation of mRNA levels for phosphacan (3-fold) and neurocan (2-fold), whereas brevican mRNA was downregulated (2-fold). Immunofluorescent signal for phosphacan and neurocan was more intense in astrocytes close to the injury site, while brevican was scarcely present in cultured astrocytes. Conclusions: Obtained results indicate that CSPGs are differentially expressed by astrocytes after scratch wounding, demonstrating that the scratch wound model might be suitable for investigation of astrocyte-derived response to injury., Uvod: Brojni in vivo i in vitro modeli opisani su sa ciljem da se rasvetle patobiološki procesi koji su osnova traumatske povrede mozga (TPM) i testiraju potencijalni tretmani. Imajući u vidu da je TPM kompleksno oboljenje, ovi modeli se međusobno razlikuju shodno aspektu TPM koji se ispituje. Jedan od in vitro modela je i povreda ćelijskog jednosloja grebanjem (engl. 'scratch wound' assay), isprva ustanovljen kao ponovljiv, jeftin test za analizu celijske migracije in vitro. Cilj ove studije je da se bliže ispita relevantnost ovog modela u odnosu na in vivo modele TPM. Metode: Da bi se istražio odgovor astrocita na mehaničku povredu, praćena je ekspresija odabranih hondroitin-sulfatnih proteoglikana (CSPG) - fosfakana, neurokana i brevikana, korišćenjem PCR u realnom vremenu i imunocitohemije. Rezultati: Dobijeni rezultati su pokazali da in vitro povreda astrocitnog jednosloja menja profile ekspresije ispitivanih CSPG. Četiri sata nakon povrede, primena PCR u realnom vremenu analize pokazala je povećanje nivoa iRNK za fosfakan (trostruko) i neurokan (dvostruko), dok je iRNK za brevikan bila smanjena na polovinu kontrolne vrednosti. Imunofluorescentni signal poreklom od fosfakana i neurokana je bio intenzivniji u astrocitima bližim mestu povrede, dok je signal za brevikan bio slab kako u kontrolnoj, tako i u ozleđenoj grupi. Zaključak: Dobijeni rezultati pokazuju da povreda izazvana grebanjem različito utiče na ekspresiju ispitivanih CSPG u astrocitima, sto ukazuju da ovaj model može biti pogodan za ispitivanje odgovora astrocita na povredu.",
journal = "Journal of Medical Biochemistry",
title = "PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi, Real-time PCR and immunocytochemical study of chondroitin sulfate proteoglycans after scratch wounding in cultured astrocytes",
number = "4",
volume = "32",
pages = "398-405",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_507"
}

Savić, D., Parabucki, A., Bjelobaba, I., Santrač, A., Dacić, S., Peković, S.,& Stojiljković, M.. (2013). PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi. in Journal of Medical Biochemistry, 32(4), 398-405.
https://hdl.handle.net/21.15107/rcub_ibiss_507

Savić D, Parabucki A, Bjelobaba I, Santrač A, Dacić S, Peković S, Stojiljković M. PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi. in Journal of Medical Biochemistry. 2013;32(4):398-405.
https://hdl.handle.net/21.15107/rcub_ibiss_507 .

Savić, Danijela, Parabucki, Ana, Bjelobaba, Ivana, Santrač, Anja, Dacić, Sanja, Peković, Sanja, Stojiljković, Mirjana, "PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi" in Journal of Medical Biochemistry, 32, no. 4 (2013):398-405,
https://hdl.handle.net/21.15107/rcub_ibiss_507 .

TY  - JOUR
AU  - Savić, Danijela
AU  - Lavrnja, Irena
AU  - Dacić, Sanja
AU  - Bjelobaba, Ivana
AU  - Nedeljković, Nadežda
AU  - Peković, Sanja
AU  - Stojiljković, Mirjana
PY  - 2012
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/317
AB  - Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), a human inflammatory and demyelinating disease. Microglia and astrocytes are glial cells of the central nervous system (CNS) that play a dual role in MS and EAE pathology. The aim of this study was to examine the effect of combined treatment with two nucleoside analogues, ribavirin and tiazofurin, on microglia and astrocytes in actively induced EAE. Therapeutic treatment with a combination of these two nucleoside analogues reduced disease severity, mononuclear cell infiltration and demyelination. The obtained histological results indicate that ribavirin and tiazofurin changed activated microglia into an inactive type and attenuated astrocyte reactivity at the end of the treatment period. Since reduction of reactive microgliosis and astrogliosis correlated with EAE suppression, the present study also suggests that the obtained beneficial effect of ribavirin and tiazofurin could be a consequence of their action inside as well as outside the CNS.
T2  - Archives of Biological Sciences
T1  - Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis
IS  - 3
VL  - 64
SP  - 843
EP  - 850
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_317
ER  - 

@article{
author = "Savić, Danijela and Lavrnja, Irena and Dacić, Sanja and Bjelobaba, Ivana and Nedeljković, Nadežda and Peković, Sanja and Stojiljković, Mirjana",
year = "2012, 2012",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), a human inflammatory and demyelinating disease. Microglia and astrocytes are glial cells of the central nervous system (CNS) that play a dual role in MS and EAE pathology. The aim of this study was to examine the effect of combined treatment with two nucleoside analogues, ribavirin and tiazofurin, on microglia and astrocytes in actively induced EAE. Therapeutic treatment with a combination of these two nucleoside analogues reduced disease severity, mononuclear cell infiltration and demyelination. The obtained histological results indicate that ribavirin and tiazofurin changed activated microglia into an inactive type and attenuated astrocyte reactivity at the end of the treatment period. Since reduction of reactive microgliosis and astrogliosis correlated with EAE suppression, the present study also suggests that the obtained beneficial effect of ribavirin and tiazofurin could be a consequence of their action inside as well as outside the CNS.",
journal = "Archives of Biological Sciences",
title = "Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis",
number = "3",
volume = "64",
pages = "843-850",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_317"
}

Savić, D., Lavrnja, I., Dacić, S., Bjelobaba, I., Nedeljković, N., Peković, S.,& Stojiljković, M.. (2012). Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis. in Archives of Biological Sciences, 64(3), 843-850.
https://hdl.handle.net/21.15107/rcub_ibiss_317

Savić D, Lavrnja I, Dacić S, Bjelobaba I, Nedeljković N, Peković S, Stojiljković M. Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis. in Archives of Biological Sciences. 2012;64(3):843-850.
https://hdl.handle.net/21.15107/rcub_ibiss_317 .

Savić, Danijela, Lavrnja, Irena, Dacić, Sanja, Bjelobaba, Ivana, Nedeljković, Nadežda, Peković, Sanja, Stojiljković, Mirjana, "Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis" in Archives of Biological Sciences, 64, no. 3 (2012):843-850,
https://hdl.handle.net/21.15107/rcub_ibiss_317 .

TY  - CONF
AU  - Parabucki, Ana
AU  - Korać, Bato
AU  - Otašević, Vesna
AU  - Bjelobaba, Ivana
AU  - Lavrnja, Irena
AU  - Stojiljković, Mirjana
AU  - Nedeljković, Nadežda
PY  - 2009
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6064
AB  - Povreda mozga obuhvata primarnu povredu, koja nastaje kao rezultat
neposrednog mehaničkog oštećenja tkiva i sekundarnu povredu koja se javlja tokom
perioda od narednih nekoliko dana. Iako još uvek nisu poznati svi detalji mehanizama
koji dovode do sekundarne povrede, nekoliko metaboličkih promena, uključujući i
povećanje produkcije reaktivnih kiseoničnih vrsta (ROS) dovedeno je u vezu sa
patofiziologijom sekundarne povrede. Budući da su mitohondrije primarno
unutarćelijsko mesto nastanka ROS, pretpostavlja se da mangan superoksid dismutaza
(MnSOD, SOD2) ima presudnu zaštitnu ulogu u antioksidativnim mehanizmima
odbrane i preživljavanju nervnih ćelija nakon povrede. Stoga je u ovom radu praćena
ekspresija MnSOD u modelu unilateralne ablacije korteksa pacova, sa ciljem da se
rasvetli njena uloga u ranim događajima nakon povrede mozga.
Svi eksperimenti izvedeni su na pacovima soja Wistar starim tri meseca.
Životinjama je pod anestezijom Zoletilom, uklonjen senzomotorni korteks na levoj
strani, pažljivim usisavanjem tkiva kroz polipropilenski vrh. Životinje se žrtvovane 0, 4,
24 i 72 časa nakon povrede i tkivo levog (LCtx) i desnog (RCtx) korteksa disecirano je i
iskorišćeno za pripremu tkivnih homogenata. Za svaku eksprimentalnu tačku, korišćena
je grupa lažno operisanih životinja, dok su neoperisane, intaktne životinje primenjene
kao fiziološka kontrola. Intenzitet signala ekspresije iRNK i proteina kod povređenih
životinja izražen je u odnosu na lažno-operisane životinje, dok je intenzitet dobijen kod
intaktnih životinja arbitrarno definisan kao 1.00.
RtPCR analiza demonstrirala je da u LCtx dolazi do rane indukcije iRNK za
MnSOD između 4 i 24 h nakon povrede. Uočeno vremenski-zavisno povećanje iRNK za
MnSOD bilo je najveće 4 sata nakon povrede. Saglasno tome, imunoblot analiza
pokazala je da je ekspresija MnSOD proteina u LCtx značajno povećana tokom prva
četiri sata nakon povrede. Ekspresija iRNK i MnSOD proteina vraća se na fiziološki
nivo 72 sata nakon povrede. S druge strane, ekspresija MnSOD, kako na nivou iRNK,
tako i na nivou proteina, ne menja se u RCtx tokom celog eksperimentalnog perioda.
Rezultati ovog rada ukazuju da povreda mozga dovodi do brzog i značajnog
povećanja ekspresije MnSOD na mestu povrede, najverovatnije kao deo odgovora na
oksidativni stres uzrokovan primarnom povredom. Budući da MnSOD predstavlja prvu
liniju odbrane od superoksid anjon radikala koji nastaju u mitohondrijama, ovi nalazi
mogu doprineti boljem razumevanju uloge MnSOD u procesu oporavka nakon povrede.
AB  - Brain injury consists of primary injury that is the result of immediate
mechanical damage and secondary injury that evolves over a period of minutes and
days. The precise mechanisms underlying secondary injury are not well understood,
however several metabolic dearangements, including increased generation of reactive
oxygen species (ROS) have been implicated in the pathophysiology following brain
damage. Since mitochondria are the major subcellular site of ROS generation,
manganese superoxid dismutase (MnSOD, SOD2), a potent scavanger of superoxide
radicals could have critical cytoprotective role in the antioxidant defence mechanism and
neuronal survival after brain damage. Thus, in the present study we have evaluated
expression of MnSOD to address its role during early events of brain injury using a
model of unilateral cortical ablation in rat.
Experiments were performed on three-month old Wistar male rats. The
sensomotory cortex was unilaterally removed on the left side by gentle suction
aspiration through polypropilene tip under the Zoletil anesthesia. Animals were
sacrificed 0, 4, 24 and 72 hours after the surgery and left (LCtx) and right (RCtx)
cortical tissues were immediately isolated for tissue homogenate preparations. For each
time point, another group of aged-matched animals was used as sham-operated controls,
whereas non-operated, intact animals were used as a physiological control. Signal
intensities obtained for MnSOD mRNA and protein expression in injured animals were
expressed relative to that obtained for sham-operated animals at each time point after the
surgery, whereas signal intensity obtained for intact control was arbitrarily defined as
1.00.
RtPCR analysis showed a rapid induction of MnSOD mRNA in LCtx between 4
and 24 h after the injury. Observed time-dependent increase in MnSOD mRNA was
maximal 4 hours after the injury compared to the level induced by sham operation alone.
Accordingly, immunoblot analysis demonstrated increased expression of MnSOD
protein in LCtx up to 4 h after the injury. 72 hours after the injury MnSOD mRNA and
protein expression return to the level of the intact control. On the other hand, MnSOD
mRNA and protein expression remained unaffected in the RCtx at all time points after
the surgery.
In conclusion, the result of this study demonstrate that brain injury induce rapid
and marked increase in MnSOD expression at the site of injury, most likely as a
protective response after oxidative stress initiated by primary brain damage. Since
MnSOD provides the first line of defense against superoxide generated in mitochondria,
these findings may contribute to a better understanding of role MnSOD in the recovery
process following brain injury.
PB  - Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology
C3  - Knjiga sažetaka: Naučni simpozijum: Mitohondrije i slobodni radikali - nov izazov; 2009 Sep 21; Belgrade, Serbia
T1  - Rano povećanje ekspresije mangan superoksid dismutaze nakon eksperimentalne povrede mozga pacova
SP  - 58
EP  - 59
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6064
ER  - 

@conference{
author = "Parabucki, Ana and Korać, Bato and Otašević, Vesna and Bjelobaba, Ivana and Lavrnja, Irena and Stojiljković, Mirjana and Nedeljković, Nadežda",
year = "2009",
abstract = "Povreda mozga obuhvata primarnu povredu, koja nastaje kao rezultat
neposrednog mehaničkog oštećenja tkiva i sekundarnu povredu koja se javlja tokom
perioda od narednih nekoliko dana. Iako još uvek nisu poznati svi detalji mehanizama
koji dovode do sekundarne povrede, nekoliko metaboličkih promena, uključujući i
povećanje produkcije reaktivnih kiseoničnih vrsta (ROS) dovedeno je u vezu sa
patofiziologijom sekundarne povrede. Budući da su mitohondrije primarno
unutarćelijsko mesto nastanka ROS, pretpostavlja se da mangan superoksid dismutaza
(MnSOD, SOD2) ima presudnu zaštitnu ulogu u antioksidativnim mehanizmima
odbrane i preživljavanju nervnih ćelija nakon povrede. Stoga je u ovom radu praćena
ekspresija MnSOD u modelu unilateralne ablacije korteksa pacova, sa ciljem da se
rasvetli njena uloga u ranim događajima nakon povrede mozga.
Svi eksperimenti izvedeni su na pacovima soja Wistar starim tri meseca.
Životinjama je pod anestezijom Zoletilom, uklonjen senzomotorni korteks na levoj
strani, pažljivim usisavanjem tkiva kroz polipropilenski vrh. Životinje se žrtvovane 0, 4,
24 i 72 časa nakon povrede i tkivo levog (LCtx) i desnog (RCtx) korteksa disecirano je i
iskorišćeno za pripremu tkivnih homogenata. Za svaku eksprimentalnu tačku, korišćena
je grupa lažno operisanih životinja, dok su neoperisane, intaktne životinje primenjene
kao fiziološka kontrola. Intenzitet signala ekspresije iRNK i proteina kod povređenih
životinja izražen je u odnosu na lažno-operisane životinje, dok je intenzitet dobijen kod
intaktnih životinja arbitrarno definisan kao 1.00.
RtPCR analiza demonstrirala je da u LCtx dolazi do rane indukcije iRNK za
MnSOD između 4 i 24 h nakon povrede. Uočeno vremenski-zavisno povećanje iRNK za
MnSOD bilo je najveće 4 sata nakon povrede. Saglasno tome, imunoblot analiza
pokazala je da je ekspresija MnSOD proteina u LCtx značajno povećana tokom prva
četiri sata nakon povrede. Ekspresija iRNK i MnSOD proteina vraća se na fiziološki
nivo 72 sata nakon povrede. S druge strane, ekspresija MnSOD, kako na nivou iRNK,
tako i na nivou proteina, ne menja se u RCtx tokom celog eksperimentalnog perioda.
Rezultati ovog rada ukazuju da povreda mozga dovodi do brzog i značajnog
povećanja ekspresije MnSOD na mestu povrede, najverovatnije kao deo odgovora na
oksidativni stres uzrokovan primarnom povredom. Budući da MnSOD predstavlja prvu
liniju odbrane od superoksid anjon radikala koji nastaju u mitohondrijama, ovi nalazi
mogu doprineti boljem razumevanju uloge MnSOD u procesu oporavka nakon povrede., Brain injury consists of primary injury that is the result of immediate
mechanical damage and secondary injury that evolves over a period of minutes and
days. The precise mechanisms underlying secondary injury are not well understood,
however several metabolic dearangements, including increased generation of reactive
oxygen species (ROS) have been implicated in the pathophysiology following brain
damage. Since mitochondria are the major subcellular site of ROS generation,
manganese superoxid dismutase (MnSOD, SOD2), a potent scavanger of superoxide
radicals could have critical cytoprotective role in the antioxidant defence mechanism and
neuronal survival after brain damage. Thus, in the present study we have evaluated
expression of MnSOD to address its role during early events of brain injury using a
model of unilateral cortical ablation in rat.
Experiments were performed on three-month old Wistar male rats. The
sensomotory cortex was unilaterally removed on the left side by gentle suction
aspiration through polypropilene tip under the Zoletil anesthesia. Animals were
sacrificed 0, 4, 24 and 72 hours after the surgery and left (LCtx) and right (RCtx)
cortical tissues were immediately isolated for tissue homogenate preparations. For each
time point, another group of aged-matched animals was used as sham-operated controls,
whereas non-operated, intact animals were used as a physiological control. Signal
intensities obtained for MnSOD mRNA and protein expression in injured animals were
expressed relative to that obtained for sham-operated animals at each time point after the
surgery, whereas signal intensity obtained for intact control was arbitrarily defined as
1.00.
RtPCR analysis showed a rapid induction of MnSOD mRNA in LCtx between 4
and 24 h after the injury. Observed time-dependent increase in MnSOD mRNA was
maximal 4 hours after the injury compared to the level induced by sham operation alone.
Accordingly, immunoblot analysis demonstrated increased expression of MnSOD
protein in LCtx up to 4 h after the injury. 72 hours after the injury MnSOD mRNA and
protein expression return to the level of the intact control. On the other hand, MnSOD
mRNA and protein expression remained unaffected in the RCtx at all time points after
the surgery.
In conclusion, the result of this study demonstrate that brain injury induce rapid
and marked increase in MnSOD expression at the site of injury, most likely as a
protective response after oxidative stress initiated by primary brain damage. Since
MnSOD provides the first line of defense against superoxide generated in mitochondria,
these findings may contribute to a better understanding of role MnSOD in the recovery
process following brain injury.",
publisher = "Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology",
journal = "Knjiga sažetaka: Naučni simpozijum: Mitohondrije i slobodni radikali - nov izazov; 2009 Sep 21; Belgrade, Serbia",
title = "Rano povećanje ekspresije mangan superoksid dismutaze nakon eksperimentalne povrede mozga pacova",
pages = "58-59",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6064"
}

Parabucki, A., Korać, B., Otašević, V., Bjelobaba, I., Lavrnja, I., Stojiljković, M.,& Nedeljković, N.. (2009). Rano povećanje ekspresije mangan superoksid dismutaze nakon eksperimentalne povrede mozga pacova. in Knjiga sažetaka: Naučni simpozijum: Mitohondrije i slobodni radikali - nov izazov; 2009 Sep 21; Belgrade, Serbia
Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology., 58-59.
https://hdl.handle.net/21.15107/rcub_ibiss_6064

Parabucki A, Korać B, Otašević V, Bjelobaba I, Lavrnja I, Stojiljković M, Nedeljković N. Rano povećanje ekspresije mangan superoksid dismutaze nakon eksperimentalne povrede mozga pacova. in Knjiga sažetaka: Naučni simpozijum: Mitohondrije i slobodni radikali - nov izazov; 2009 Sep 21; Belgrade, Serbia. 2009;:58-59.
https://hdl.handle.net/21.15107/rcub_ibiss_6064 .

Parabucki, Ana, Korać, Bato, Otašević, Vesna, Bjelobaba, Ivana, Lavrnja, Irena, Stojiljković, Mirjana, Nedeljković, Nadežda, "Rano povećanje ekspresije mangan superoksid dismutaze nakon eksperimentalne povrede mozga pacova" in Knjiga sažetaka: Naučni simpozijum: Mitohondrije i slobodni radikali - nov izazov; 2009 Sep 21; Belgrade, Serbia (2009):58-59,
https://hdl.handle.net/21.15107/rcub_ibiss_6064 .

TY  - JOUR
AU  - Dacić, Sanja
AU  - Peković, Sanja
AU  - Stojiljković, Maja T.
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Bjelobaba, Ivana
AU  - Stojiljković, Mirjana
PY  - 2008
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/207
AB  - The central nervous system has a limited capacity for self-repair after damage. However, the neonatal brain has agreater capacity for recovery than the adult brain. These differences in the regenerative capability depend on local environmental factors and the maturational stage of growing axons. Among molecules which have both growth-promoting and growth-inhibiting activities is the heterogeneous class of chondroitin sulfate proteoglycans (CSPGs). In this paper, we investigated the chondroitin-4 and chondroitin-6 sulfate proteoglycan expression profile after left sensorimotor cortex ablation of the neonatal and adult rat brain. Immunohistochemical analysis revealed that compared to the normal uninjured cortex, lesion provoked up regulation of CSPGs showing a different pattern of expression in the neonatal vs. the adult brain. Punctuate and membrane-bound labeling was predominate after neonatal lesion, where as heavy deposition of staining in the extracellular matrix was observed after adult lesion. Heavy deposition of CSPG immunoreactivity around the lesionsite in adult rats, in contrast to a less CSPG-rich environment in neonatal rats, indicated that enhancement of the recovery process after neonatal injury is due to amore permissive environment.
AB  - Centralni nervni sistem ima ograničen kapacitet za oporavak nakon povrede. Međutim, neonatalni mozak pokazuje veću sposobnost oporavka u odnosu na odrasle. Ove razlike zavise od lokalnih sredinskih faktora i stepena zrelosti aksona tokom izrastanja. U grupu molekula koji mogu da stimulišu ili inhibiraju rast aksona spada i heterogena klasa molekula označena kao hondroitin sulfatni proteoglikani (CSPG). U ovom radu ispitivanje profil ekspresije hondroitin-4 i hondroitin-6 sulfatnih proteoglikana nakonlezije leve senzomotorne kore neonatalnog i adultnog mozga pacova. Imunohistohemijska analiza pokazuje da u odnosu na normalni,nepovređeni korteks, lezija dovodi do povećanja ekspresije CSPG koji ima različiti obrazac promena u neonatalnom u odnosu na adultni mozak. Nakonlezije kod mladih, predominiraju tačkasta i membranski-vezana forma, dok kod odraslih lezija dovodi do nagomilavanja CSPG u ekstra ćelijskom matriksu. Prohodnija sredina u mozgu neonatalnih pacova koja je siromašnija CSPG, preduslov je boljeg procesa oporavka u odnosu na adulte, kod kojih se nakon povrede CSPG nagomilavaju oko mesta lezije.
T2  - Archives of Biological Sciences
T1  - Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova
T1  - Pattern of chondroitin sulfate proteoglycan expression after ablation of the sensorimotor cortex of the neonatal and adult rat brain
IS  - 4
VL  - 60
SP  - 581
EP  - 591
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_207
ER  - 

@article{
author = "Dacić, Sanja and Peković, Sanja and Stojiljković, Maja T. and Lavrnja, Irena and Savić, Danijela and Bjelobaba, Ivana and Stojiljković, Mirjana",
year = "2008, 2008",
abstract = "The central nervous system has a limited capacity for self-repair after damage. However, the neonatal brain has agreater capacity for recovery than the adult brain. These differences in the regenerative capability depend on local environmental factors and the maturational stage of growing axons. Among molecules which have both growth-promoting and growth-inhibiting activities is the heterogeneous class of chondroitin sulfate proteoglycans (CSPGs). In this paper, we investigated the chondroitin-4 and chondroitin-6 sulfate proteoglycan expression profile after left sensorimotor cortex ablation of the neonatal and adult rat brain. Immunohistochemical analysis revealed that compared to the normal uninjured cortex, lesion provoked up regulation of CSPGs showing a different pattern of expression in the neonatal vs. the adult brain. Punctuate and membrane-bound labeling was predominate after neonatal lesion, where as heavy deposition of staining in the extracellular matrix was observed after adult lesion. Heavy deposition of CSPG immunoreactivity around the lesionsite in adult rats, in contrast to a less CSPG-rich environment in neonatal rats, indicated that enhancement of the recovery process after neonatal injury is due to amore permissive environment., Centralni nervni sistem ima ograničen kapacitet za oporavak nakon povrede. Međutim, neonatalni mozak pokazuje veću sposobnost oporavka u odnosu na odrasle. Ove razlike zavise od lokalnih sredinskih faktora i stepena zrelosti aksona tokom izrastanja. U grupu molekula koji mogu da stimulišu ili inhibiraju rast aksona spada i heterogena klasa molekula označena kao hondroitin sulfatni proteoglikani (CSPG). U ovom radu ispitivanje profil ekspresije hondroitin-4 i hondroitin-6 sulfatnih proteoglikana nakonlezije leve senzomotorne kore neonatalnog i adultnog mozga pacova. Imunohistohemijska analiza pokazuje da u odnosu na normalni,nepovređeni korteks, lezija dovodi do povećanja ekspresije CSPG koji ima različiti obrazac promena u neonatalnom u odnosu na adultni mozak. Nakonlezije kod mladih, predominiraju tačkasta i membranski-vezana forma, dok kod odraslih lezija dovodi do nagomilavanja CSPG u ekstra ćelijskom matriksu. Prohodnija sredina u mozgu neonatalnih pacova koja je siromašnija CSPG, preduslov je boljeg procesa oporavka u odnosu na adulte, kod kojih se nakon povrede CSPG nagomilavaju oko mesta lezije.",
journal = "Archives of Biological Sciences",
title = "Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova, Pattern of chondroitin sulfate proteoglycan expression after ablation of the sensorimotor cortex of the neonatal and adult rat brain",
number = "4",
volume = "60",
pages = "581-591",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_207"
}

Dacić, S., Peković, S., Stojiljković, M. T., Lavrnja, I., Savić, D., Bjelobaba, I.,& Stojiljković, M.. (2008). Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova. in Archives of Biological Sciences, 60(4), 581-591.
https://hdl.handle.net/21.15107/rcub_ibiss_207

Dacić S, Peković S, Stojiljković MT, Lavrnja I, Savić D, Bjelobaba I, Stojiljković M. Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova. in Archives of Biological Sciences. 2008;60(4):581-591.
https://hdl.handle.net/21.15107/rcub_ibiss_207 .

Dacić, Sanja, Peković, Sanja, Stojiljković, Maja T., Lavrnja, Irena, Savić, Danijela, Bjelobaba, Ivana, Stojiljković, Mirjana, "Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova" in Archives of Biological Sciences, 60, no. 4 (2008):581-591,
https://hdl.handle.net/21.15107/rcub_ibiss_207 .

TY  - CHAP
AU  - Peković, Sanja
AU  - Dacić, Sanja
AU  - Nedeljković, Nadežda
AU  - Bjelobaba, Ivana
AU  - Filipović, Radmila
AU  - Milenković, Ivan
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Jovanović, Saša
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2006
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5871
AB  - Injury to the central nervous system (CNS) is one of the leading causes of death and invalidity among all people below the age of 45 for which there are no specific treatments. The insight into the molecular pathophysiology of brain dysfunctions after the injury will provide indications for new effective therapeutic approaches that will limit damage, slow cell death and promote repair. The aim of this review is to highlight molecular mechanisms underlining primary and secondary injury. The initial impact or primary injury induces elevation of extracellular concentration of neurotransmitters leading to changes in electrical properties of neuronal membrane, net influx of Ca2+ and activation of diverse cellular signaling pathways. To restore neuronal homeostasis, the activities and expression of a variety of enzymes involved in control of extracellular concentration of biogenic amines and purine nucleotides/nucleosides, as well as the membrane potential are altered. The CNS has a limited capacity of self-repair. However, there are indications that the neonatal brain has a greater capacity for recovery than adult brain. The well known pathological hallmark of CNS injury is formation of the glial scar, the major impediment to axonal regeneration. Recently, it was shown that treatment with the purine nucleoside analogues attenuates and delays the process of reactive gliosis, and thus may be a useful approach for improving neurological recovery from head injury.
PB  - Kerala, India: Research Signpost
T2  - Neurobiological studies – From genes to behavior 2006
T1  - Molecular basis of brain injury and repair
SP  - 143
EP  - 165
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5871
ER  - 

@inbook{
author = "Peković, Sanja and Dacić, Sanja and Nedeljković, Nadežda and Bjelobaba, Ivana and Filipović, Radmila and Milenković, Ivan and Lavrnja, Irena and Savić, Danijela and Jovanović, Saša and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2006",
abstract = "Injury to the central nervous system (CNS) is one of the leading causes of death and invalidity among all people below the age of 45 for which there are no specific treatments. The insight into the molecular pathophysiology of brain dysfunctions after the injury will provide indications for new effective therapeutic approaches that will limit damage, slow cell death and promote repair. The aim of this review is to highlight molecular mechanisms underlining primary and secondary injury. The initial impact or primary injury induces elevation of extracellular concentration of neurotransmitters leading to changes in electrical properties of neuronal membrane, net influx of Ca2+ and activation of diverse cellular signaling pathways. To restore neuronal homeostasis, the activities and expression of a variety of enzymes involved in control of extracellular concentration of biogenic amines and purine nucleotides/nucleosides, as well as the membrane potential are altered. The CNS has a limited capacity of self-repair. However, there are indications that the neonatal brain has a greater capacity for recovery than adult brain. The well known pathological hallmark of CNS injury is formation of the glial scar, the major impediment to axonal regeneration. Recently, it was shown that treatment with the purine nucleoside analogues attenuates and delays the process of reactive gliosis, and thus may be a useful approach for improving neurological recovery from head injury.",
publisher = "Kerala, India: Research Signpost",
journal = "Neurobiological studies – From genes to behavior 2006",
booktitle = "Molecular basis of brain injury and repair",
pages = "143-165",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5871"
}

Peković, S., Dacić, S., Nedeljković, N., Bjelobaba, I., Filipović, R., Milenković, I., Lavrnja, I., Savić, D., Jovanović, S., Rakić, L.,& Stojiljković, M.. (2006). Molecular basis of brain injury and repair. in Neurobiological studies – From genes to behavior 2006
Kerala, India: Research Signpost., 143-165.
https://hdl.handle.net/21.15107/rcub_ibiss_5871

Peković S, Dacić S, Nedeljković N, Bjelobaba I, Filipović R, Milenković I, Lavrnja I, Savić D, Jovanović S, Rakić L, Stojiljković M. Molecular basis of brain injury and repair. in Neurobiological studies – From genes to behavior 2006. 2006;:143-165.
https://hdl.handle.net/21.15107/rcub_ibiss_5871 .

Peković, Sanja, Dacić, Sanja, Nedeljković, Nadežda, Bjelobaba, Ivana, Filipović, Radmila, Milenković, Ivan, Lavrnja, Irena, Savić, Danijela, Jovanović, Saša, Rakić, Ljubisav, Stojiljković, Mirjana, "Molecular basis of brain injury and repair" in Neurobiological studies – From genes to behavior 2006 (2006):143-165,
https://hdl.handle.net/21.15107/rcub_ibiss_5871 .

TY  - JOUR
AU  - Savić, Danijela
AU  - Lavrnja, Irena
AU  - Šubašić, Sanja
AU  - Bjelobaba, Ivana
AU  - Peković, Sanja
AU  - Gađanski, Ivana
AU  - Mostarica-Stojković, Marija B
AU  - Stošić-Grujičić, Stanislava
AU  - Rakić, Lj.
AU  - Stojiljković, Mirjana
PY  - 2006
PY  - 2006
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/127
AB  - Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model of the human neurological disorder multiple sclerosis. The purpose of the present study was to investigate the effect of combined treatment with two nucleoside analogs, ribavirin and tiazofurin, on development of EAE actively induced in highly susceptible dark agouti rats. The obtained results showed that ribavirin and tiazofurin applied either separately or in combination from the onset of the firstsymptoms of EAE after its induction (therapeutic treatment) significantly suppressed EAE’s clinical symptoms. However, the most pronounced effect was gained with combined treatment, probably as a result of synergistic/additive action.
AB  - Eksperimentalni autoimunski encefalomijelitis (EAE) je animalni model koji se obično koristi kao prototip humanog neurološkog oboljenja - multiple skleroze. Cilj ove studije bio je ispitivanje efekta kombinovane terapije sa dva nukleozidna analoga, ribavirina i tiazofurina, na razvoj EAE, aktivno izazvanog kod veoma osetljivog dark aguti soja pacova. Dobijeni rezultati pokazali su da ribavirin i tiazofurin, primenjeni pojedinačno ili u kombinaciji, od pojave prvog simptoma EAE (terapijski tretman), značajno suprimiraju težinu ove bolesti. Međutim, najbolji efekti su postignuti kombinovanim tretmanom, što je verovatno posledica sinergističkog ili aditivnog delovanja ribavirina i tiazofurina.
T2  - Archives of Biological Sciences
T1  - Terapijski efekat nukleozidnih analoga na eksperimentalni autoimunski encefalomijelitis kod dark agouti pacova
T1  - Therapeutic effect of nucleoside analogs on experimental autoimmune encephalomyelitis in dark agouti rats
IS  - 1
VL  - 58
SP  - 13
EP  - 20
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_127
ER  - 

@article{
author = "Savić, Danijela and Lavrnja, Irena and Šubašić, Sanja and Bjelobaba, Ivana and Peković, Sanja and Gađanski, Ivana and Mostarica-Stojković, Marija B and Stošić-Grujičić, Stanislava and Rakić, Lj. and Stojiljković, Mirjana",
year = "2006, 2006",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model of the human neurological disorder multiple sclerosis. The purpose of the present study was to investigate the effect of combined treatment with two nucleoside analogs, ribavirin and tiazofurin, on development of EAE actively induced in highly susceptible dark agouti rats. The obtained results showed that ribavirin and tiazofurin applied either separately or in combination from the onset of the firstsymptoms of EAE after its induction (therapeutic treatment) significantly suppressed EAE’s clinical symptoms. However, the most pronounced effect was gained with combined treatment, probably as a result of synergistic/additive action., Eksperimentalni autoimunski encefalomijelitis (EAE) je animalni model koji se obično koristi kao prototip humanog neurološkog oboljenja - multiple skleroze. Cilj ove studije bio je ispitivanje efekta kombinovane terapije sa dva nukleozidna analoga, ribavirina i tiazofurina, na razvoj EAE, aktivno izazvanog kod veoma osetljivog dark aguti soja pacova. Dobijeni rezultati pokazali su da ribavirin i tiazofurin, primenjeni pojedinačno ili u kombinaciji, od pojave prvog simptoma EAE (terapijski tretman), značajno suprimiraju težinu ove bolesti. Međutim, najbolji efekti su postignuti kombinovanim tretmanom, što je verovatno posledica sinergističkog ili aditivnog delovanja ribavirina i tiazofurina.",
journal = "Archives of Biological Sciences",
title = "Terapijski efekat nukleozidnih analoga na eksperimentalni autoimunski encefalomijelitis kod dark agouti pacova, Therapeutic effect of nucleoside analogs on experimental autoimmune encephalomyelitis in dark agouti rats",
number = "1",
volume = "58",
pages = "13-20",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_127"
}

Savić, D., Lavrnja, I., Šubašić, S., Bjelobaba, I., Peković, S., Gađanski, I., Mostarica-Stojković, M. B., Stošić-Grujičić, S., Rakić, Lj.,& Stojiljković, M.. (2006). Terapijski efekat nukleozidnih analoga na eksperimentalni autoimunski encefalomijelitis kod dark agouti pacova. in Archives of Biological Sciences, 58(1), 13-20.
https://hdl.handle.net/21.15107/rcub_ibiss_127

Savić D, Lavrnja I, Šubašić S, Bjelobaba I, Peković S, Gađanski I, Mostarica-Stojković MB, Stošić-Grujičić S, Rakić L, Stojiljković M. Terapijski efekat nukleozidnih analoga na eksperimentalni autoimunski encefalomijelitis kod dark agouti pacova. in Archives of Biological Sciences. 2006;58(1):13-20.
https://hdl.handle.net/21.15107/rcub_ibiss_127 .

Savić, Danijela, Lavrnja, Irena, Šubašić, Sanja, Bjelobaba, Ivana, Peković, Sanja, Gađanski, Ivana, Mostarica-Stojković, Marija B, Stošić-Grujičić, Stanislava, Rakić, Lj., Stojiljković, Mirjana, "Terapijski efekat nukleozidnih analoga na eksperimentalni autoimunski encefalomijelitis kod dark agouti pacova" in Archives of Biological Sciences, 58, no. 1 (2006):13-20,
https://hdl.handle.net/21.15107/rcub_ibiss_127 .

TY  - JOUR
AU  - Peković, Sanja
AU  - Filipović, Radmila
AU  - Dacić, Sanja
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Nedeljković, Nadežda
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2005
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5870
AB  - The weak regenerative capacity of self-repair after injury to the adult brain is caused by the formation of glial sear due to reactive astrogliosis. In the present study the beginning of reactive astrogliosis in the adult, as shown immunocytochemically by upregulation of glial fibrillary acidic protein (GFAP) and vimentin, was seen two days after the left sensorimotor cortex lesion, being maximal during the first two weeks and declining by 30 days after the lesion. This was accompanied by intensive glial scarring. Conversely, after the neonatal lesion a lack of gliotic scar was seen until 30 days postsurgery, although the pattern of GFAP and vimentin expression during recovery period was the same. The aim of the study was to define an appropriate therapeutic intervention that could modulate astrocyte proliferation and diminish glial scar formation after adult brain lesion. For this purpose the effects of an antiproliferative agent, the purine nucleoside analogue ribavirin was examined. It was shown that daily injection of ribavirin for 5 and 10 days considerably decreased the number of reactive astrocytes, while slight GFAP labeling was restricted to the lesion site. Obtained results show that ribavirin treatment downregulates the process of reactive astrogliosis after adult brain injury, and thus may be a useful approach for improving neurological recovery from brain damage.
PB  - Hoboken, NJ: Wiley
T2  - Annals of the New York Academy of Sciences
T1  - Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin
IS  - 1
VL  - 1048
DO  - 10.1196/annals.1342.027
SP  - 296
EP  - 310
ER  - 

@article{
author = "Peković, Sanja and Filipović, Radmila and Dacić, Sanja and Lavrnja, Irena and Savić, Danijela and Nedeljković, Nadežda and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2005",
abstract = "The weak regenerative capacity of self-repair after injury to the adult brain is caused by the formation of glial sear due to reactive astrogliosis. In the present study the beginning of reactive astrogliosis in the adult, as shown immunocytochemically by upregulation of glial fibrillary acidic protein (GFAP) and vimentin, was seen two days after the left sensorimotor cortex lesion, being maximal during the first two weeks and declining by 30 days after the lesion. This was accompanied by intensive glial scarring. Conversely, after the neonatal lesion a lack of gliotic scar was seen until 30 days postsurgery, although the pattern of GFAP and vimentin expression during recovery period was the same. The aim of the study was to define an appropriate therapeutic intervention that could modulate astrocyte proliferation and diminish glial scar formation after adult brain lesion. For this purpose the effects of an antiproliferative agent, the purine nucleoside analogue ribavirin was examined. It was shown that daily injection of ribavirin for 5 and 10 days considerably decreased the number of reactive astrocytes, while slight GFAP labeling was restricted to the lesion site. Obtained results show that ribavirin treatment downregulates the process of reactive astrogliosis after adult brain injury, and thus may be a useful approach for improving neurological recovery from brain damage.",
publisher = "Hoboken, NJ: Wiley",
journal = "Annals of the New York Academy of Sciences",
title = "Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin",
number = "1",
volume = "1048",
doi = "10.1196/annals.1342.027",
pages = "296-310"
}

Peković, S., Filipović, R., Dacić, S., Lavrnja, I., Savić, D., Nedeljković, N., Rakić, L.,& Stojiljković, M.. (2005). Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin. in Annals of the New York Academy of Sciences
Hoboken, NJ: Wiley., 1048(1), 296-310.
https://doi.org/10.1196/annals.1342.027

Peković S, Filipović R, Dacić S, Lavrnja I, Savić D, Nedeljković N, Rakić L, Stojiljković M. Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin. in Annals of the New York Academy of Sciences. 2005;1048(1):296-310.
doi:10.1196/annals.1342.027 .

Peković, Sanja, Filipović, Radmila, Dacić, Sanja, Lavrnja, Irena, Savić, Danijela, Nedeljković, Nadežda, Rakić, Ljubisav, Stojiljković, Mirjana, "Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin" in Annals of the New York Academy of Sciences, 1048, no. 1 (2005):296-310,
https://doi.org/10.1196/annals.1342.027 . .

TY  - JOUR
AU  - Petković, Branka
AU  - Pešić, Vesna
AU  - Peković, Sanja
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2005
UR  - https://link.springer.com/article/10.1007%2Fs00221-005-2311-0
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3809
AB  - The time-course of changes of basal and amphetamine (AMPH)-induced locomotor and stereotypic activities in adult male Wistar rats after a single ribavirin injection was studied. In the first set of experiments, 10, 20 or 30 mg ribavirin/kg body weight (b.w.) were injected i.p. to rats and their basal motor activities were recorded every 10 min for 2 h and compared with those of saline-treated controls. In the second set of experiments, the animals were pretreated with ribavirin and 20 min later i.p. injected with AMPH (1.5 mg/kg b.w.). The controls received AMPH 20 min after the saline injection. Motor activity was recorded after the first injection and until 120 min after AMPH administration. Ribavirin did not significantly affect the time-course of either basal locomotor or stereotypic activities. Pretreatment with any of the applied ribavirin doses decreased the AMPH-induced hyperlocomotor response. However, the most pronounced effect was observed with ribavirin doses of 20 mg/kg and 30 mg/kg when administered during the first 10 min and 30 min after the AMPH injection respectively. In contrast, the stereotypic activities of these animals were only slightly changed. These results indicate a different susceptibility of regions in the basal ganglia to ribavirin.
PB  - Springer
T2  - Experimental Brain Research
T1  - The time-course of ribavirin-provoked changes of basal and AMPH-induced motor activities in rats
IS  - 3
VL  - 165
DO  - 10.1007/s00221-005-2311-0
SP  - 402
EP  - 406
ER  - 

@article{
author = "Petković, Branka and Pešić, Vesna and Peković, Sanja and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2005",
abstract = "The time-course of changes of basal and amphetamine (AMPH)-induced locomotor and stereotypic activities in adult male Wistar rats after a single ribavirin injection was studied. In the first set of experiments, 10, 20 or 30 mg ribavirin/kg body weight (b.w.) were injected i.p. to rats and their basal motor activities were recorded every 10 min for 2 h and compared with those of saline-treated controls. In the second set of experiments, the animals were pretreated with ribavirin and 20 min later i.p. injected with AMPH (1.5 mg/kg b.w.). The controls received AMPH 20 min after the saline injection. Motor activity was recorded after the first injection and until 120 min after AMPH administration. Ribavirin did not significantly affect the time-course of either basal locomotor or stereotypic activities. Pretreatment with any of the applied ribavirin doses decreased the AMPH-induced hyperlocomotor response. However, the most pronounced effect was observed with ribavirin doses of 20 mg/kg and 30 mg/kg when administered during the first 10 min and 30 min after the AMPH injection respectively. In contrast, the stereotypic activities of these animals were only slightly changed. These results indicate a different susceptibility of regions in the basal ganglia to ribavirin.",
publisher = "Springer",
journal = "Experimental Brain Research",
title = "The time-course of ribavirin-provoked changes of basal and AMPH-induced motor activities in rats",
number = "3",
volume = "165",
doi = "10.1007/s00221-005-2311-0",
pages = "402-406"
}

Petković, B., Pešić, V., Peković, S., Rakić, L.,& Stojiljković, M.. (2005). The time-course of ribavirin-provoked changes of basal and AMPH-induced motor activities in rats. in Experimental Brain Research
Springer., 165(3), 402-406.
https://doi.org/10.1007/s00221-005-2311-0

Petković B, Pešić V, Peković S, Rakić L, Stojiljković M. The time-course of ribavirin-provoked changes of basal and AMPH-induced motor activities in rats. in Experimental Brain Research. 2005;165(3):402-406.
doi:10.1007/s00221-005-2311-0 .

Petković, Branka, Pešić, Vesna, Peković, Sanja, Rakić, Ljubisav, Stojiljković, Mirjana, "The time-course of ribavirin-provoked changes of basal and AMPH-induced motor activities in rats" in Experimental Brain Research, 165, no. 3 (2005):402-406,
https://doi.org/10.1007/s00221-005-2311-0 . .

TY  - JOUR
AU  - Pešić, Vesna
AU  - Veskov, Rosica
AU  - Petković, Branka
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2003
UR  - https://www.sciencedirect.com/science/article/abs/pii/S0197458002002324?via%3Dihub
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3812
AB  - Changes in locomotor and stereotypic activities induced by an i.p. injection of either (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)-cycloheptan-5,10- imine maleate (dizocilpine or MK-801; 0.3 mg/kg) or D-amphetamine sulfate (AMPH; 1.5 mg/kg) were studied in male Mill Hill hooded rats of different age. The following age groups of animals were considered: 28-30 postnatal day (PND)-old rats (peripubertal), 48-50 PND-old (pubertal), 3-month-old (adults), 12-month-old (middle-aged) and 24-month-old (aged). The motor response was measured by an automated animal activity measuring system. The obtained results showed that: (1) in contrast to AMPH, MK-801 induced more pronounced increases of both locomotor and stereotypic activities in peripubertal and pubertal than in adult and aged rats; (2) AMPH induced the same locomotor and stereotypic activity increase in pubertal, adult and middle-aged rats; (3) both AMPH and MK-801 led to a senescence-related decrease of motor activity. These data suggest that the balance of the glutamatergic and dopaminergic systems changes during aging. Such a change is important in understanding schizophrenia and the motor system decline observed in the later stages of life.
PB  - Elsevier Science Inc
T2  - Neurobiology of Aging
T1  - Age-related differences in MK-801- and amphetamine-induced locomotor and stereotypic activities of rats
IS  - 5
VL  - 24
DO  - 10.1016/S0197-4580(02)00232-4
SP  - 715
EP  - 723
ER  - 

@article{
author = "Pešić, Vesna and Veskov, Rosica and Petković, Branka and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2003",
abstract = "Changes in locomotor and stereotypic activities induced by an i.p. injection of either (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)-cycloheptan-5,10- imine maleate (dizocilpine or MK-801; 0.3 mg/kg) or D-amphetamine sulfate (AMPH; 1.5 mg/kg) were studied in male Mill Hill hooded rats of different age. The following age groups of animals were considered: 28-30 postnatal day (PND)-old rats (peripubertal), 48-50 PND-old (pubertal), 3-month-old (adults), 12-month-old (middle-aged) and 24-month-old (aged). The motor response was measured by an automated animal activity measuring system. The obtained results showed that: (1) in contrast to AMPH, MK-801 induced more pronounced increases of both locomotor and stereotypic activities in peripubertal and pubertal than in adult and aged rats; (2) AMPH induced the same locomotor and stereotypic activity increase in pubertal, adult and middle-aged rats; (3) both AMPH and MK-801 led to a senescence-related decrease of motor activity. These data suggest that the balance of the glutamatergic and dopaminergic systems changes during aging. Such a change is important in understanding schizophrenia and the motor system decline observed in the later stages of life.",
publisher = "Elsevier Science Inc",
journal = "Neurobiology of Aging",
title = "Age-related differences in MK-801- and amphetamine-induced locomotor and stereotypic activities of rats",
number = "5",
volume = "24",
doi = "10.1016/S0197-4580(02)00232-4",
pages = "715-723"
}

Pešić, V., Veskov, R., Petković, B., Rakić, L.,& Stojiljković, M.. (2003). Age-related differences in MK-801- and amphetamine-induced locomotor and stereotypic activities of rats. in Neurobiology of Aging
Elsevier Science Inc., 24(5), 715-723.
https://doi.org/10.1016/S0197-4580(02)00232-4

Pešić V, Veskov R, Petković B, Rakić L, Stojiljković M. Age-related differences in MK-801- and amphetamine-induced locomotor and stereotypic activities of rats. in Neurobiology of Aging. 2003;24(5):715-723.
doi:10.1016/S0197-4580(02)00232-4 .

Pešić, Vesna, Veskov, Rosica, Petković, Branka, Rakić, Ljubisav, Stojiljković, Mirjana, "Age-related differences in MK-801- and amphetamine-induced locomotor and stereotypic activities of rats" in Neurobiology of Aging, 24, no. 5 (2003):715-723,
https://doi.org/10.1016/S0197-4580(02)00232-4 . .