Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex
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2012
Authors
Đorđević, Ana D.Đorđević, Jelena D.
Elaković, Ivana
Adžić, Miroslav
Matić, Gordana
Radojčić, Marija
Article (Published version)
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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.
Keywords:
Stress / Prefrontal cortex / Plasticity / Apoptosis / Antidepressant fluoxetineSource:
European Journal of Pharmacology, 2012, 693, 1-3, 37-44Funding / projects:
- Defining a cluster of molecular biomarkers for improved diagnostics and therapy of mood disorders (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41029)
- Role of steroid hormones in neuroendocrine adaptation to stress and pathophysiology of metabolic syndrome - molecular mechanisms and clinical implications (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41009)
DOI: 10.1016/j.ejphar.2012.07.042
ISSN: 0014-2999; 1879-0712
PubMed: 22959317
WoS: 000308918600006
Scopus: 2-s2.0-84866281766
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VinčaTY - 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 . .