TY  - JOUR
AU  - Matić, Gordana
AU  - Milutinovic, Danijela Vojnovic
AU  - Nestorov, Jelena
AU  - Elaković, Ivana
AU  - Jovanovic, Sanja Manitasevic
AU  - Elzaedi, Younis Mouftah
AU  - Perisic, Tatjana
AU  - Dunderski, Jadranka
AU  - Damjanović, Svetozar S.
AU  - Knežević, Goran
AU  - Spiric, Zeljko
AU  - Vermetten, Eric
AU  - Savić, Danka A.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5909
AB  - Alterations in the number and functional status of mineralocorticoid (MR) and glucocorticoid receptors (GR) may contribute to vulnerability to posttraumatic stress disorder (PTSD). Corticosteroid receptors are chaperoned by heat shock proteins Hsp90 and Hsp70. We examined relations between corticosteroid receptor and heat shock protein expression levels, and related them with war trauma exposure, PTSD and resilience to PTSD. Relative levels of MR. Hsp90 and Hsp70 were determined by immunoblotting in lymphocytes from war trauma-exposed men with current PTSD (current PTSD group, n=113), with lifetime PTSD (life-time PTSD group, n=61) and without PTSD (trauma control group, n=88), and from non-traumatized healthy controls (healthy control group, n=85). Between-group differences in MR, Hsp90 and Hsp70 levels and in MR/GR ratio were not observed. The level of MR was correlated with both Hsp90 and Hsp70 levels in trauma control and healthy control groups. On the other hand, GR level was correlated only with Hsp90 level, and this correlation was evident in current PTSD and trauma control groups. In conclusion, PTSD and exposure to trauma are not related to changes in lymphocyte MR, Hsp90 or Hsp70 levels, but may be associated with disturbances in corticosteroid receptors interaction with heat shock proteins. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
T2  - Psychiatry Research
T1  - Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD
VL  - 215
IS  - 2
SP  - 379
EP  - 385
DO  - 10.1016/j.psychres.2013.11.022
ER  - 

@article{
author = "Matić, Gordana and Milutinovic, Danijela Vojnovic and Nestorov, Jelena and Elaković, Ivana and Jovanovic, Sanja Manitasevic and Elzaedi, Younis Mouftah and Perisic, Tatjana and Dunderski, Jadranka and Damjanović, Svetozar S. and Knežević, Goran and Spiric, Zeljko and Vermetten, Eric and Savić, Danka A.",
year = "2014",
abstract = "Alterations in the number and functional status of mineralocorticoid (MR) and glucocorticoid receptors (GR) may contribute to vulnerability to posttraumatic stress disorder (PTSD). Corticosteroid receptors are chaperoned by heat shock proteins Hsp90 and Hsp70. We examined relations between corticosteroid receptor and heat shock protein expression levels, and related them with war trauma exposure, PTSD and resilience to PTSD. Relative levels of MR. Hsp90 and Hsp70 were determined by immunoblotting in lymphocytes from war trauma-exposed men with current PTSD (current PTSD group, n=113), with lifetime PTSD (life-time PTSD group, n=61) and without PTSD (trauma control group, n=88), and from non-traumatized healthy controls (healthy control group, n=85). Between-group differences in MR, Hsp90 and Hsp70 levels and in MR/GR ratio were not observed. The level of MR was correlated with both Hsp90 and Hsp70 levels in trauma control and healthy control groups. On the other hand, GR level was correlated only with Hsp90 level, and this correlation was evident in current PTSD and trauma control groups. In conclusion, PTSD and exposure to trauma are not related to changes in lymphocyte MR, Hsp90 or Hsp70 levels, but may be associated with disturbances in corticosteroid receptors interaction with heat shock proteins. (C) 2013 Elsevier Ireland Ltd. All rights reserved.",
journal = "Psychiatry Research",
title = "Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD",
volume = "215",
number = "2",
pages = "379-385",
doi = "10.1016/j.psychres.2013.11.022"
}

Matić, G., Milutinovic, D. V., Nestorov, J., Elaković, I., Jovanovic, S. M., Elzaedi, Y. M., Perisic, T., Dunderski, J., Damjanović, S. S., Knežević, G., Spiric, Z., Vermetten, E.,& Savić, D. A.. (2014). Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD. in Psychiatry Research, 215(2), 379-385.
https://doi.org/10.1016/j.psychres.2013.11.022

Matić G, Milutinovic DV, Nestorov J, Elaković I, Jovanovic SM, Elzaedi YM, Perisic T, Dunderski J, Damjanović SS, Knežević G, Spiric Z, Vermetten E, Savić DA. Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD. in Psychiatry Research. 2014;215(2):379-385.
doi:10.1016/j.psychres.2013.11.022 .

Matić, Gordana, Milutinovic, Danijela Vojnovic, Nestorov, Jelena, Elaković, Ivana, Jovanovic, Sanja Manitasevic, Elzaedi, Younis Mouftah, Perisic, Tatjana, Dunderski, Jadranka, Damjanović, Svetozar S., Knežević, Goran, Spiric, Zeljko, Vermetten, Eric, Savić, Danka A., "Mineralocorticoid receptor and heat shock protein expression levels in peripheral lymphocytes from war trauma-exposed men with and without PTSD" in Psychiatry Research, 215, no. 2 (2014):379-385,
https://doi.org/10.1016/j.psychres.2013.11.022 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Lukić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Đorđević, Ana D.
AU  - Krstić-Demonacos, Marija
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5868
AB  - Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.
T2  - Psychoneuroendocrinology
T1  - Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism
VL  - 38
IS  - 12
SP  - 2914
EP  - 2924
DO  - 10.1016/j.psyneuen.2013.07.019
ER  - 

@article{
author = "Adžić, Miroslav and Lukić, Iva and Mitić, Miloš and Đorđević, Jelena D. and Elaković, Ivana and Đorđević, Ana D. and Krstić-Demonacos, Marija and Matić, Gordana and Radojčić, Marija",
year = "2013",
abstract = "Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.",
journal = "Psychoneuroendocrinology",
title = "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism",
volume = "38",
number = "12",
pages = "2914-2924",
doi = "10.1016/j.psyneuen.2013.07.019"
}

Adžić, M., Lukić, I., Mitić, M., Đorđević, J. D., Elaković, I., Đorđević, A. D., Krstić-Demonacos, M., Matić, G.,& Radojčić, M.. (2013). Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology, 38(12), 2914-2924.
https://doi.org/10.1016/j.psyneuen.2013.07.019

Adžić M, Lukić I, Mitić M, Đorđević JD, Elaković I, Đorđević AD, Krstić-Demonacos M, Matić G, Radojčić M. Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology. 2013;38(12):2914-2924.
doi:10.1016/j.psyneuen.2013.07.019 .

Adžić, Miroslav, Lukić, Iva, Mitić, Miloš, Đorđević, Jelena D., Elaković, Ivana, Đorđević, Ana D., Krstić-Demonacos, Marija, Matić, Gordana, Radojčić, Marija, "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism" in Psychoneuroendocrinology, 38, no. 12 (2013):2914-2924,
https://doi.org/10.1016/j.psyneuen.2013.07.019 . .

TY  - JOUR
AU  - Matić, Gordana
AU  - Milutinovic, Danijela Vojnovic
AU  - Nestorov, Jelena
AU  - Elaković, Ivana
AU  - Jovanovic, Sanja Manitasevic
AU  - Perisic, Tatjana
AU  - Dunderski, Jadranka
AU  - Damjanović, Svetozar S.
AU  - Knežević, Goran
AU  - Spiric, Zeljko
AU  - Vermetten, Eric
AU  - Savić, Danka A.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5429
AB  - Objective: Posttraumatic stress disorder (PTSD) has been shown to be associated with altered glucocorticoid receptor (GR) activity. We studied the expression and functional properties of the receptor in peripheral blood mononuclear cells (PBMCs) from non-traumatized healthy individuals (healthy controls; n = 85), and war trauma-exposed individuals with current PTSD (n = 113), with life-time PTSD (n = 61) and without PTSD (trauma controls; n = 88). The aim of the study was to distinguish the receptor alterations related to PTSD from those related to trauma itself or to resilience to PTSD. Methods: Functional status of the receptor was assessed by radioligand binding and lysozyme synthesis inhibition assays. The level of GR gene expression was measured by quantitative PCR and immunoblotting. Results: Current PTSD patients had the lowest, while trauma controls had the highest number of glucocorticoid binding sites (B-max) in PBMCs. Hormone-binding potential (B-max/K-D ratio) of the receptor was diminished in the current PTSD group in comparison to all other study groups. Correlation between B-max and K-D that normally exists in healthy individuals was decreased in the current PTSD group. Contrasting B-max data, GR protein level was lower in trauma controls than in participants with current or life-time PTSD. Conclusions: Current PTSD is characterized by reduced lymphocyte GR hormone-binding potential and by disturbed compensation between B-max and hormone-binding affinity. Resilience to PTSD is associated with enlarged fraction of the receptor molecules capable of hormone binding, within the total receptor molecule population in PBMCs. (C) 2013 Elsevier Inc. All rights reserved.
T2  - Progress in Neuro-psychopharmacology and Biological Psychiatry
T1  - Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD
VL  - 43
SP  - 238
EP  - 245
DO  - 10.1016/j.pnpbp.2013.01.005
ER  - 

@article{
author = "Matić, Gordana and Milutinovic, Danijela Vojnovic and Nestorov, Jelena and Elaković, Ivana and Jovanovic, Sanja Manitasevic and Perisic, Tatjana and Dunderski, Jadranka and Damjanović, Svetozar S. and Knežević, Goran and Spiric, Zeljko and Vermetten, Eric and Savić, Danka A.",
year = "2013",
abstract = "Objective: Posttraumatic stress disorder (PTSD) has been shown to be associated with altered glucocorticoid receptor (GR) activity. We studied the expression and functional properties of the receptor in peripheral blood mononuclear cells (PBMCs) from non-traumatized healthy individuals (healthy controls; n = 85), and war trauma-exposed individuals with current PTSD (n = 113), with life-time PTSD (n = 61) and without PTSD (trauma controls; n = 88). The aim of the study was to distinguish the receptor alterations related to PTSD from those related to trauma itself or to resilience to PTSD. Methods: Functional status of the receptor was assessed by radioligand binding and lysozyme synthesis inhibition assays. The level of GR gene expression was measured by quantitative PCR and immunoblotting. Results: Current PTSD patients had the lowest, while trauma controls had the highest number of glucocorticoid binding sites (B-max) in PBMCs. Hormone-binding potential (B-max/K-D ratio) of the receptor was diminished in the current PTSD group in comparison to all other study groups. Correlation between B-max and K-D that normally exists in healthy individuals was decreased in the current PTSD group. Contrasting B-max data, GR protein level was lower in trauma controls than in participants with current or life-time PTSD. Conclusions: Current PTSD is characterized by reduced lymphocyte GR hormone-binding potential and by disturbed compensation between B-max and hormone-binding affinity. Resilience to PTSD is associated with enlarged fraction of the receptor molecules capable of hormone binding, within the total receptor molecule population in PBMCs. (C) 2013 Elsevier Inc. All rights reserved.",
journal = "Progress in Neuro-psychopharmacology and Biological Psychiatry",
title = "Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD",
volume = "43",
pages = "238-245",
doi = "10.1016/j.pnpbp.2013.01.005"
}

Matić, G., Milutinovic, D. V., Nestorov, J., Elaković, I., Jovanovic, S. M., Perisic, T., Dunderski, J., Damjanović, S. S., Knežević, G., Spiric, Z., Vermetten, E.,& Savić, D. A.. (2013). Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD. in Progress in Neuro-psychopharmacology and Biological Psychiatry, 43, 238-245.
https://doi.org/10.1016/j.pnpbp.2013.01.005

Matić G, Milutinovic DV, Nestorov J, Elaković I, Jovanovic SM, Perisic T, Dunderski J, Damjanović SS, Knežević G, Spiric Z, Vermetten E, Savić DA. Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD. in Progress in Neuro-psychopharmacology and Biological Psychiatry. 2013;43:238-245.
doi:10.1016/j.pnpbp.2013.01.005 .

Matić, Gordana, Milutinovic, Danijela Vojnovic, Nestorov, Jelena, Elaković, Ivana, Jovanovic, Sanja Manitasevic, Perisic, Tatjana, Dunderski, Jadranka, Damjanović, Svetozar S., Knežević, Goran, Spiric, Zeljko, Vermetten, Eric, Savić, Danka A., "Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD" in Progress in Neuro-psychopharmacology and Biological Psychiatry, 43 (2013):238-245,
https://doi.org/10.1016/j.pnpbp.2013.01.005 . .

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radoičić, Marija B.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4678
AB  - Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Progress in Neuro-psychopharmacology and Biological Psychiatry
T1  - Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats
VL  - 36
IS  - 1
SP  - 92
EP  - 100
DO  - 10.1016/j.pnpbp.2011.10.006
ER  - 

@article{
author = "Đorđević, Ana D. and Đorđević, Jelena D. and Elaković, Ivana and Adžić, Miroslav and Matić, Gordana and Radoičić, Marija B.",
year = "2012",
abstract = "Plastic response and successful adaptation to stress are of particular importance in the hippocampus, where chronic stress may cause cell death instead of neural remodeling. Structural modifications that occur both in the brain of depressed patients and animal stress models may be reversed by antidepressants. Since morphological changes induced by stress and/or antidepressants could be mediated by presynaptically located proteins, determining the levels of these proteins may be a useful way to identify molecular changes associated with synaptic plasticity. In this study we analyzed the effects of chronic (six-week) social isolation and long-term (three-week) fluoxetine treatment on molecular markers of plasticity and apoptosis in the hippocampus of Wistar rats. Compartmental redistribution of NF kappa B transcription factor involved in the regulation of plasticity and apoptosis was also examined. To establish whether social isolation is able to evoke behavioral-like effects, which might be related to the observed molecular changes, we performed the forced swimming test. The results show that synaptosomal polysialic neural cell adhesion molecule (PSA-NCAM), a molecular plasticity marker, was increased in the hippocampus of chronically isolated rats, while subsequent treatment with fluoxetine set it at the control level. In addition, analysis of cytoplasm/mitochondria redistribution of apoptotic proteins Bax and Bcl-2 after exposure to chronic isolation stress, revealed an increase in Bcl-2 protein expression in both compartments, while fluoxetine enhanced the effect of stress only in the mitochondria. The observed alterations at the molecular level were accompanied by normalization of stress-induced behavioral changes by fluoxetine. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Progress in Neuro-psychopharmacology and Biological Psychiatry",
title = "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats",
volume = "36",
number = "1",
pages = "92-100",
doi = "10.1016/j.pnpbp.2011.10.006"
}

Đorđević, A. D., Đorđević, J. D., Elaković, I., Adžić, M., Matić, G.,& Radoičić, M. B.. (2012). Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. in Progress in Neuro-psychopharmacology and Biological Psychiatry, 36(1), 92-100.
https://doi.org/10.1016/j.pnpbp.2011.10.006

Đorđević AD, Đorđević JD, Elaković I, Adžić M, Matić G, Radoičić MB. Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats. in Progress in Neuro-psychopharmacology and Biological Psychiatry. 2012;36(1):92-100.
doi:10.1016/j.pnpbp.2011.10.006 .

Đorđević, Ana D., Đorđević, Jelena D., Elaković, Ivana, Adžić, Miroslav, Matić, Gordana, Radoičić, Marija B., "Fluoxetine affects hippocampal plasticity, apoptosis and depressive-like behavior of chronically isolated rats" in Progress in Neuro-psychopharmacology and Biological Psychiatry, 36, no. 1 (2012):92-100,
https://doi.org/10.1016/j.pnpbp.2011.10.006 . .

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5042
AB  - The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex
VL  - 693
IS  - 1-3
SP  - 37
EP  - 44
DO  - 10.1016/j.ejphar.2012.07.042
ER  - 

@article{
author = "Đorđević, Ana D. and Đorđević, Jelena D. and Elaković, Ivana and Adžić, Miroslav and Matić, Gordana and Radojčić, Marija",
year = "2012",
abstract = "The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex",
volume = "693",
number = "1-3",
pages = "37-44",
doi = "10.1016/j.ejphar.2012.07.042"
}

Đorđević, A. D., Đorđević, J. D., Elaković, I., Adžić, M., Matić, G.,& Radojčić, M.. (2012). Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology, 693(1-3), 37-44.
https://doi.org/10.1016/j.ejphar.2012.07.042

Đorđević AD, Đorđević JD, Elaković I, Adžić M, Matić G, Radojčić M. Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology. 2012;693(1-3):37-44.
doi:10.1016/j.ejphar.2012.07.042 .

Đorđević, Ana D., Đorđević, Jelena D., Elaković, Ivana, Adžić, Miroslav, Matić, Gordana, Radojčić, Marija, "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex" in European Journal of Pharmacology, 693, no. 1-3 (2012):37-44,
https://doi.org/10.1016/j.ejphar.2012.07.042 . .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4329
AB  - Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver
VL  - 659
IS  - 1
SP  - 61
EP  - 66
DO  - 10.1016/j.ejphar.2011.03.003
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Elaković, Ivana and Matić, Gordana and Radojčić, Marija",
year = "2011",
abstract = "Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver",
volume = "659",
number = "1",
pages = "61-66",
doi = "10.1016/j.ejphar.2011.03.003"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M., Elaković, I., Matić, G.,& Radojčić, M.. (2011). Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. in European Journal of Pharmacology, 659(1), 61-66.
https://doi.org/10.1016/j.ejphar.2011.03.003

Đorđević JD, Đorđević AD, Adžić M, Elaković I, Matić G, Radojčić M. Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. in European Journal of Pharmacology. 2011;659(1):61-66.
doi:10.1016/j.ejphar.2011.03.003 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Elaković, Ivana, Matić, Gordana, Radojčić, Marija, "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver" in European Journal of Pharmacology, 659, no. 1 (2011):61-66,
https://doi.org/10.1016/j.ejphar.2011.03.003 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Rackov, Gorjana
AU  - Đorđević, Ana D.
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4640
AB  - Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.
T2  - Acta Chimica Slovenica
T1  - Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats
VL  - 58
IS  - 4
SP  - 785
EP  - 791
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4640
ER  - 

@article{
author = "Adžić, Miroslav and Đorđević, Jelena D. and Mitić, Miloš and Simić, Iva and Rackov, Gorjana and Đorđević, Ana D. and Elaković, Ivana and Matić, Gordana and Radojčić, Marija",
year = "2011",
abstract = "Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.",
journal = "Acta Chimica Slovenica",
title = "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats",
volume = "58",
number = "4",
pages = "785-791",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4640"
}

Adžić, M., Đorđević, J. D., Mitić, M., Simić, I., Rackov, G., Đorđević, A. D., Elaković, I., Matić, G.,& Radojčić, M.. (2011). Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. in Acta Chimica Slovenica, 58(4), 785-791.
https://hdl.handle.net/21.15107/rcub_vinar_4640

Adžić M, Đorđević JD, Mitić M, Simić I, Rackov G, Đorđević AD, Elaković I, Matić G, Radojčić M. Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. in Acta Chimica Slovenica. 2011;58(4):785-791.
https://hdl.handle.net/21.15107/rcub_vinar_4640 .

Adžić, Miroslav, Đorđević, Jelena D., Mitić, Miloš, Simić, Iva, Rackov, Gorjana, Đorđević, Ana D., Elaković, Ivana, Matić, Gordana, Radojčić, Marija, "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats" in Acta Chimica Slovenica, 58, no. 4 (2011):785-791,
https://hdl.handle.net/21.15107/rcub_vinar_4640 .

TY  - JOUR
AU  - Elaković, Ivana
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
AU  - Matić, Gordana
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4277
AB  - Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.
T2  - Brain Research
T1  - Gender-specific response of brain corticosteroid receptors to stress and fluoxetine
VL  - 1384
SP  - 61
EP  - 68
DO  - 10.1016/j.brainres.2011.01.078
ER  - 

@article{
author = "Elaković, Ivana and Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radojčić, Marija and Matić, Gordana",
year = "2011",
abstract = "Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "Brain Research",
title = "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine",
volume = "1384",
pages = "61-68",
doi = "10.1016/j.brainres.2011.01.078"
}

Elaković, I., Đorđević, A. D., Adžić, M., Đorđević, J. D., Radojčić, M.,& Matić, G.. (2011). Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. in Brain Research, 1384, 61-68.
https://doi.org/10.1016/j.brainres.2011.01.078

Elaković I, Đorđević AD, Adžić M, Đorđević JD, Radojčić M, Matić G. Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. in Brain Research. 2011;1384:61-68.
doi:10.1016/j.brainres.2011.01.078 .

Elaković, Ivana, Đorđević, Ana D., Adžić, Miroslav, Đorđević, Jelena D., Radojčić, Marija, Matić, Gordana, "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine" in Brain Research, 1384 (2011):61-68,
https://doi.org/10.1016/j.brainres.2011.01.078 . .

TY  - JOUR
AU  - Elaković, Ivana
AU  - Vasiljević, Đorđe
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3960
AB  - Gender-related differences in the expression and functional properties of the hepatic glucocorticoid receptor were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Some of the receptors functional properties, including hormone-binding capacity (B-max), hormone-binding potency (B-max/K-D ratio) and the DNA-binding ability, were found to be sexually dimorphic. Fluoxetine treatment (5 mg/kg body mass, 21 day, intraperitoneally) induced a decrease in B-max and in the amount of Hsp70 co-immunoprecipitated with the glucocorticoid receptor only in males, and stimulated the association of the receptor with Hsp90 in females. When applied during the last three weeks of the 6-week isolation, fluoxetine parallelly elevated B-max and the receptor protein level in female animals, while in males diminished B-max and inhibited association of the receptor with Hsp70. Binding of dexamethasone-receptor complexes both to DNA-cellulose and to isolated liver nuclei did not appear to be a target for fluoxetine action. The results point to sex-related differences in the glucocorticoid receptor functioning and in its response to fluoxetine, and suggest that these differences may contribute to well known sexual dimorphism in the sensitivity to stress, to stress-related disorders and to antidepressant treatment. (C) 2010 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine
VL  - 632
IS  - 1-3
SP  - 79
EP  - 85
DO  - 10.1016/j.ejphar.2010.01.015
ER  - 

@article{
author = "Elaković, Ivana and Vasiljević, Đorđe and Adžić, Miroslav and Đorđević, Ana D. and Đorđević, Jelena D. and Matić, Gordana and Radojčić, Marija",
year = "2010",
abstract = "Gender-related differences in the expression and functional properties of the hepatic glucocorticoid receptor were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Some of the receptors functional properties, including hormone-binding capacity (B-max), hormone-binding potency (B-max/K-D ratio) and the DNA-binding ability, were found to be sexually dimorphic. Fluoxetine treatment (5 mg/kg body mass, 21 day, intraperitoneally) induced a decrease in B-max and in the amount of Hsp70 co-immunoprecipitated with the glucocorticoid receptor only in males, and stimulated the association of the receptor with Hsp90 in females. When applied during the last three weeks of the 6-week isolation, fluoxetine parallelly elevated B-max and the receptor protein level in female animals, while in males diminished B-max and inhibited association of the receptor with Hsp70. Binding of dexamethasone-receptor complexes both to DNA-cellulose and to isolated liver nuclei did not appear to be a target for fluoxetine action. The results point to sex-related differences in the glucocorticoid receptor functioning and in its response to fluoxetine, and suggest that these differences may contribute to well known sexual dimorphism in the sensitivity to stress, to stress-related disorders and to antidepressant treatment. (C) 2010 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine",
volume = "632",
number = "1-3",
pages = "79-85",
doi = "10.1016/j.ejphar.2010.01.015"
}

Elaković, I., Vasiljević, Đ., Adžić, M., Đorđević, A. D., Đorđević, J. D., Matić, G.,& Radojčić, M.. (2010). Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine. in European Journal of Pharmacology, 632(1-3), 79-85.
https://doi.org/10.1016/j.ejphar.2010.01.015

Elaković I, Vasiljević Đ, Adžić M, Đorđević AD, Đorđević JD, Matić G, Radojčić M. Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine. in European Journal of Pharmacology. 2010;632(1-3):79-85.
doi:10.1016/j.ejphar.2010.01.015 .

Elaković, Ivana, Vasiljević, Đorđe, Adžić, Miroslav, Đorđević, Ana D., Đorđević, Jelena D., Matić, Gordana, Radojčić, Marija, "Sexually dimorphic functional alterations of rat hepatic glucocorticoid receptor in response to fluoxetine" in European Journal of Pharmacology, 632, no. 1-3 (2010):79-85,
https://doi.org/10.1016/j.ejphar.2010.01.015 . .