Gender-specific effects of fluoxetine on hippocampal glucocorticoid receptor phosphorylation and behavior in chronically stressed rats

Mitić, Miloš; Simic, Iva; Djordjević, Jelena; Radojčić, Marija B.; Adžić, Miroslav

doi:10.1016/j.neuropharm.2012.12.012

Cited by 46 publications

(38 citation statements)

References 117 publications

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“…The lack of effect or an opposite effect in control animals is commonly observed in pharmacological treatments (Mitic et al 2013;Nishiyori and Ueda 2008;Lewitus et al 2009). However, the GA treatment induced an increase in CAT activity.…”

Section: Discussionmentioning

confidence: 99%

Involvement of nitric oxide in improving stress-induced behavioural alteration by glatiramer acetate treatment in female BALB/c mice

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Involvement of nitric oxide in improving stress-induced behavioural alteration by glatiramer acetate treatment in female BALB/c mice

et al. 2014

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“…Notably, such fluoxetine-induced hippocampal increase in BDNF is not consistently observed in the literature, which may be due to the variety of experimental designs (especially time of measurement) and conditions (Coppell et al, 2003; de Foubert et al, 2004; First et al, 2011;Mitic et al, 2013).…”

Section: The Journal Of Experimental Biologymentioning

confidence: 99%

Epigenetic mechanisms underlying the role of brain-derived neurotrophic factor in depression and response to antidepressants

Duclot

Kabbaj

2015

Journal of Experimental Biology

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Major depressive disorder (MDD) is a devastating neuropsychiatric disorder encompassing a wide range of cognitive and emotional dysfunctions. The prevalence of MDD is expected to continue its growth to become the second leading cause of disease burden (after HIV) by 2030. Despite an extensive research effort, the exact etiology of MDD remains elusive and the diagnostics uncertain. Moreover, a marked inter-individual variability is observed in the vulnerability to develop depression, as well as in response to antidepressant treatment, for nearly 50% of patients. Although a genetic component accounts for some cases of MDD, it is now clearly established that MDD results from strong gene and environment interactions. Such interactions could be mediated by epigenetic mechanisms, defined as chromatin and DNA modifications that alter gene expression without changing the DNA structure itself. Some epigenetic mechanisms have recently emerged as particularly relevant molecular substrates, promoting vulnerability or resilience to the development of depressive-like symptoms. Although the role of brainderived neurotrophic factor (BDNF) in the pathophysiology of MDD remains unclear, its modulation of the efficacy of antidepressants is clearly established. Therefore, in this review, we focus on the epigenetic mechanisms regulating the expression of BDNF in humans and in animal models of depression, and discuss their role in individual differences in vulnerability to depression and response to antidepressant drugs. KEY WORDS: BDNF, Epigenetics, Individual differences IntroductionMajor depressive disorder (MDD) is a common debilitating disorder (Bromet et al., 2011) affecting many aspects of the patient's life and family. In addition to its high comorbidity with other neuropsychiatric conditions and increased rate of suicide, depression has a variety of socioeconomic consequences, including low education, unstable employment, reduced work performance and marital dysfunction (Kessler and Bromet, 2013). In 2000, the economic costs of depression in the United States alone were estimated at $83.1 billion, encompassing direct medical costs, suicide-related mortality costs, as well as indirect workplace costs (Greenberg et al., 2003). Moreover, the prevalence of depressive disorders is expected to continue its growth and become by the year 2030 the second leading cause of disease burden among the World Health Organization member states (Mathers and Loncar, 2006). Despite extensive research efforts in past decades, the etiology of REVIEW Department of Biomedical Sciences, Neuroscience Program, Florida State University, Tallahassee, FL 32306, USA.*Author for correspondence (mohamed.kabbaj@med.fsu.edu) depression remains elusive, its diagnosis uncertain and the pharmacotherapy inefficient. Indeed, the antidepressants currently used, which target the monoaminergic pathways, require weeks to months of treatment and exhibit very poor or no response in nearly 50% of patients (Magni et al., 2013;Trivedi et al., 2006;Warden et al., 20...

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“…However, even animal studies from the 1990s indicated that GR of various brain regions and GR from immune system tissues are similarly regulated by corticosterone (Lowy 1991;Spencer et al 1991). Further, recent studies demon-depressants affect GR functioning via modulation of the receptor phosphorylation status (Guidotti et al 2013;Mitic et al 2013). The absence of the clinical studies related to the effects of antidepressants on activity of GR protein, particularly on its phosphorylation status, requires urgent action.…”

Section: Limitationsmentioning

confidence: 99%

“…Likewise, we have recently shown that GR phosphorylation, evaluated through levels of nuclear pGR-211 and pGR-226, was altered in patients with major depressive disorder (MDD) compared to healthy controls (Simic et al 2013a). Moreover, an animal model study from our group indicated that chronic psychosocial stress was related to the alterations in GR phosphorylation status in the nuclear extracts of the rat hippocampus and prefrontal cortex (Adzic et al 2009;Mitic et al 2013).…”

Section: Introductionmentioning

confidence: 96%

The role of glucocorticoid receptor phosphorylation in the model of negative affective states

Jovičić

Maric

Soldatović

et al. 2015

The World Journal of Biological Psychiatry

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Gender-specific effects of fluoxetine on hippocampal glucocorticoid receptor phosphorylation and behavior in chronically stressed rats

Cited by 46 publications

References 117 publications

Involvement of nitric oxide in improving stress-induced behavioural alteration by glatiramer acetate treatment in female BALB/c mice

Involvement of nitric oxide in improving stress-induced behavioural alteration by glatiramer acetate treatment in female BALB/c mice

Epigenetic mechanisms underlying the role of brain-derived neurotrophic factor in depression and response to antidepressants

The role of glucocorticoid receptor phosphorylation in the model of negative affective states

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