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Browsing by Author "Petronijevic, Natasa (6506911099)"

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    Maternal Deprivation in Rats Decreases the Expression of Interneuron Markers in the Neocortex and Hippocampus
    (2021)
    Aksic, Milan (57211016229)
    ;
    Poleksic, Joko (57193867385)
    ;
    Aleksic, Dubravka (55887215500)
    ;
    Petronijevic, Natasa (6506911099)
    ;
    Radonjic, Nevena V. (23390243000)
    ;
    Jakovcevski, Maja (57218883670)
    ;
    Kapor, Slobodan (24321238000)
    ;
    Divac, Nevena (23003936900)
    ;
    Filipovic, Branislav R. (56207614900)
    ;
    Jakovcevski, Igor (16833586200)
    Early life stress has profound effects on the development of the central nervous system. We exposed 9-day-old rat pups to a 24 h maternal deprivation (MD) and sacrificed them as young adults (60-day-old), with the aim to study the effects of early stress on forebrain circuitry. We estimated numbers of various immunohistochemically defined interneuron subpopulations in several neocortical regions and in the hippocampus. MD rats showed reduced numbers of parvalbumin-expressing interneurons in the CA1 region of the hippocampus and in the prefrontal cortex, compared with controls. Numbers of reelin-expressing and calretinin-expressing interneurons were also reduced in the CA1 and CA3 hippocampal areas, but unaltered in the neocortex of MD rats. The number of calbinin-expressing interneurons in the neocortex was similar in the MD rats compared with controls. We analyzed cell death in 15-day-old rats after MD and found no difference compared to control rats. Thus, our results more likely reflect the downregulation of markers than the actual loss of interneurons. To investigate synaptic activity in the hippocampus we immunostained for glutamatergic and inhibitory vesicular transporters. The number of inhibitory synapses was decreased in the CA1 and CA3 regions of the hippocampus in MD rats, with the normal number of excitatory synapses. Our results indicate complex, cell type-specific, and region-specific alterations in the inhibitory circuitry induced by maternal deprivation. Such alterations may underlie symptoms of MD at the behavioral level and possibly contribute to mechanisms by which early life stress causes neuropsychiatric disorders, such as schizophrenia. © Copyright © 2021 Aksic, Poleksic, Aleksic, Petronijevic, Radonjic, Jakovcevski, Kapor, Divac, Filipovic and Jakovcevski.
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    Publication
    Maternal Deprivation in Rats Decreases the Expression of Interneuron Markers in the Neocortex and Hippocampus
    (2021)
    Aksic, Milan (57211016229)
    ;
    Poleksic, Joko (57193867385)
    ;
    Aleksic, Dubravka (55887215500)
    ;
    Petronijevic, Natasa (6506911099)
    ;
    Radonjic, Nevena V. (23390243000)
    ;
    Jakovcevski, Maja (57218883670)
    ;
    Kapor, Slobodan (24321238000)
    ;
    Divac, Nevena (23003936900)
    ;
    Filipovic, Branislav R. (56207614900)
    ;
    Jakovcevski, Igor (16833586200)
    Early life stress has profound effects on the development of the central nervous system. We exposed 9-day-old rat pups to a 24 h maternal deprivation (MD) and sacrificed them as young adults (60-day-old), with the aim to study the effects of early stress on forebrain circuitry. We estimated numbers of various immunohistochemically defined interneuron subpopulations in several neocortical regions and in the hippocampus. MD rats showed reduced numbers of parvalbumin-expressing interneurons in the CA1 region of the hippocampus and in the prefrontal cortex, compared with controls. Numbers of reelin-expressing and calretinin-expressing interneurons were also reduced in the CA1 and CA3 hippocampal areas, but unaltered in the neocortex of MD rats. The number of calbinin-expressing interneurons in the neocortex was similar in the MD rats compared with controls. We analyzed cell death in 15-day-old rats after MD and found no difference compared to control rats. Thus, our results more likely reflect the downregulation of markers than the actual loss of interneurons. To investigate synaptic activity in the hippocampus we immunostained for glutamatergic and inhibitory vesicular transporters. The number of inhibitory synapses was decreased in the CA1 and CA3 regions of the hippocampus in MD rats, with the normal number of excitatory synapses. Our results indicate complex, cell type-specific, and region-specific alterations in the inhibitory circuitry induced by maternal deprivation. Such alterations may underlie symptoms of MD at the behavioral level and possibly contribute to mechanisms by which early life stress causes neuropsychiatric disorders, such as schizophrenia. © Copyright © 2021 Aksic, Poleksic, Aleksic, Petronijevic, Radonjic, Jakovcevski, Kapor, Divac, Filipovic and Jakovcevski.
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    NADPH oxidase and redox status in amygdala, hippocampus and cortex of male Wistar rats in an animal model of post-traumatic stress disorder
    (2018)
    Petrovic, Romana (57202197136)
    ;
    Puskas, Laslo (7003598901)
    ;
    Jevtic Dozudic, Gordana (55307708600)
    ;
    Stojkovic, Tihomir (55332669300)
    ;
    Velimirovic, Milica (56270007000)
    ;
    Nikolic, Tatjana (57235024600)
    ;
    Zivkovic, Milica (57221209295)
    ;
    Djorovic, Djordje J. (57202188015)
    ;
    Nenadovic, Milutin (36629072000)
    ;
    Petronijevic, Natasa (6506911099)
    Post-traumatic stress disorder (PTSD) is a highly prevalent and impairing disorder. Oxidative stress is implicated in its pathogenesis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important source of free radicals. The aim of the study was to assess oxidative stress parameters, activities of respiratory chain enzymes, and the expression of NADPH oxidase subunits (gp91phox, p22phox, and p67phox) in the single prolonged stress (SPS) animal model of PTSD. Twenty-four (12 controls; 12 subjected to SPS), 9-week-old, male Wistar rats were used. SPS included physical restraint, forced swimming, and ether exposure. The rats were euthanized seven days later. Cortex, hippocampus, amygdala, and thalamus were dissected. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), Complex I, and cytochrome C oxidase were measured using spectrophotometric methods, while the expression of NADPH oxidase subunits was determined by Western blot. Increased MDA and decreased GSH concentrations were found in the amygdala and hippocampus of the SPS rats. SOD activity was decreased in amygdala and GPx was decreased in hippocampus. Increased expression of the NADPH oxidase subunits was seen in amygdala, while mitochondrial respiratory chain enzyme expression was unchanged both in amygdala and hippocampus. In the cortex concentrations of MDA and GSH were unchanged despite increased Complex I and decreased GPx, while in the thalamus no change of any parameter was noticed. We conclude that oxidative stress is present in hippocampus and amygdala seven days after the SPS procedure. NADPH oxidase seems to be a main source of free radicals in the amygdala. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.
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    Publication
    NADPH oxidase and redox status in amygdala, hippocampus and cortex of male Wistar rats in an animal model of post-traumatic stress disorder
    (2018)
    Petrovic, Romana (57202197136)
    ;
    Puskas, Laslo (7003598901)
    ;
    Jevtic Dozudic, Gordana (55307708600)
    ;
    Stojkovic, Tihomir (55332669300)
    ;
    Velimirovic, Milica (56270007000)
    ;
    Nikolic, Tatjana (57235024600)
    ;
    Zivkovic, Milica (57221209295)
    ;
    Djorovic, Djordje J. (57202188015)
    ;
    Nenadovic, Milutin (36629072000)
    ;
    Petronijevic, Natasa (6506911099)
    Post-traumatic stress disorder (PTSD) is a highly prevalent and impairing disorder. Oxidative stress is implicated in its pathogenesis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important source of free radicals. The aim of the study was to assess oxidative stress parameters, activities of respiratory chain enzymes, and the expression of NADPH oxidase subunits (gp91phox, p22phox, and p67phox) in the single prolonged stress (SPS) animal model of PTSD. Twenty-four (12 controls; 12 subjected to SPS), 9-week-old, male Wistar rats were used. SPS included physical restraint, forced swimming, and ether exposure. The rats were euthanized seven days later. Cortex, hippocampus, amygdala, and thalamus were dissected. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), Complex I, and cytochrome C oxidase were measured using spectrophotometric methods, while the expression of NADPH oxidase subunits was determined by Western blot. Increased MDA and decreased GSH concentrations were found in the amygdala and hippocampus of the SPS rats. SOD activity was decreased in amygdala and GPx was decreased in hippocampus. Increased expression of the NADPH oxidase subunits was seen in amygdala, while mitochondrial respiratory chain enzyme expression was unchanged both in amygdala and hippocampus. In the cortex concentrations of MDA and GSH were unchanged despite increased Complex I and decreased GPx, while in the thalamus no change of any parameter was noticed. We conclude that oxidative stress is present in hippocampus and amygdala seven days after the SPS procedure. NADPH oxidase seems to be a main source of free radicals in the amygdala. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.

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