Neuronal plasticity: A link between stress and mood disorders

Calabrese, Francesca; Molteni, Raffaella; Racagni, Giorgio; Riva, Marco A.

doi:10.1016/j.psyneuen.2009.05.014

Cited by 260 publications

(175 citation statements)

References 81 publications

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“…We had previously demonstrated that chronic treatment with the SNRI antidepressant duloxetine is able to normalize Bdnf deficits in these animals, also through the modulation of Bdnf exon I and IV (Calabrese et al, 2010, present results). Such data are in agreement with the possibility that repeated, but not acute, treatment with major classes of antidepressants may improve neuronal plasticity through the modulation of Bdnf expression (Calabrese et al, 2007;Castren et al, 2007;Molteni et al, 2009a;Russo-Neustadt and Chen, 2005), and that this effect may contribute to their therapeutic action (Berton and Nestler, 2006;Calabrese et al, 2009;Calabrese et al, 2011;Groves, 2007;Martinowich et al, 2007).…”

Section: Discussionsupporting

confidence: 86%

Developmental Influence of the Serotonin Transporter on the Expression of Npas4 and GABAergic Markers: Modulation by Antidepressant Treatment

Guidotti

Calabrese

Auletta

et al. 2011

Neuropsychopharmacol

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Alterations of the serotonergic system are involved in the pathophysiology of mood disorders and represent an important target for its pharmacological treatment. Genetic deletion of the serotonin transporter (SERT) in rodents leads to an anxious and depressive phenotype, and is associated with reduced neuronal plasticity as indicated by decreased brain-derived neurotrophic factor (Bdnf) expression levels. One of the transcription factors regulating Bdnf is the neuronal PAS domain protein 4 (Npas4), which regulates activitydependent genes and neuroprotection, and has a critical role in the development of GABA synapses. On the basis of these premises, we investigated the expression of Npas4 and GABAergic markers in the hippocampus and prefrontal cortex of homozygous (SERT À/À ) and heterozygous (SERT + /À ) knockout rats, and analyzed the effect of long-term duloxetine treatment on the expression of these targets. We found that Npas4 expression was reduced in both the brain structures of adult SERT + /À and SERT À/À animals. This effect was already present in adolescent SERT À/À , and could be mimicked by prenatal exposure to the antidepressant fluoxetine. Moreover, SERT À/À rats showed a strong impairment of the GABAergic system, as indicated by the reduction of several markers, including the vesicular transporter (Vgat), glutamic acid decarboxylase-67 (Gad67), the receptor subunit GABA A receptor, gamma 2 (GABA A -g2), and calciumbinding proteins that label subgroups of the GABAergic neurons. Interestingly, chronic treatment with the antidepressant duloxetine was able to restore the physiological levels of Npas4 and GABAergic markers in SERT À/À rats, although some differences in the modulation of GABAergic genes exist between hippocampus and prefrontal cortex. Our results demonstrate that SERT knockout rats, an animal model of mood disorders, have reduced Npas4 expression that correlates with decreased expression of Bdnf exon I and IV. These changes lead to an impairment of the GABAergic system that may contribute to the anxious and depressive phenotype associated with inherited SERT downregulation.

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Section: Discussionsupporting

confidence: 86%

Developmental Influence of the Serotonin Transporter on the Expression of Npas4 and GABAergic Markers: Modulation by Antidepressant Treatment

Guidotti

Calabrese

Auletta

et al. 2011

Neuropsychopharmacol

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“…Regardless, accruing data indicate a critical role of BDNF and neuroplasticity in the vulnerability to depression (Calabrese et al, 2009;Castren et al, 2010;Sen et al, 2008); many instances of depression are strongly linked with increased inflammatory cytokines (Haroon et al, 2012;Miller et al, 2009), and there is a likely interaction between BDNF and inflammatory cytokines (Lotrich, 2012). Herein, we report that lower BDNF levels (and the Val/Met polymorphisms rs6265) can increase susceptibility to subsequent inflammatory cytokine-associated depression.…”

Section: Discussionmentioning

confidence: 71%

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

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Depression has been associated with inflammation, and inflammation may both influence and interact with growth factors such as brainderived neurotrophic factor (BDNF). Both the functional Val66Met BDNF polymorphism (rs6265) and BDNF levels have been associated with depression. It is thus plausible that decreased BDNF could mediate and/or moderate cytokine-induced depression. We therefore prospectively employed the Beck Depression Inventory-II (BDI-II), the Hospital Anxiety and Depression Scale (HADS), and the Montgomery-Asberg Depression Rating Scale (MADRS) in 124 initially euthymic patients during treatment with interferon-alpha (IFN-a), assessing serum BDNF and rs6265. Using mixed-effect repeated measures, lower pretreatment BDNF was associated with higher depression symptoms during IFN-a treatment (F 144,17.2 ¼ 6.8; Po0.0001). However, although the Met allele was associated with lower BDNF levels (F 1,83.0 ¼ 5.0; P ¼ 0.03), it was only associated with increased MADRS scores (F 4,8.9 ¼ 20.3; Po0.001), and not the BDI-II or HADS. An exploratory comparison of individual BDI-II items indicated that the Met allele was associated with suicidal ideation, sadness, and worthlessness, but not neurovegetative symptoms. Conversely, the serotonin transporter promoter polymorphism (5-HTTLPR) short allele was associated with neurovegetative symptoms such as insomnia, poor appetite and fatigue, but not sadness, worthlessness, or suicidal ideation. IFN-a therapy further lowered BDNF serum levels (F 4,37.7 ¼ 5.0; P ¼ 0.003), but this decrease occurred regardless of depression development. The findings thus do not support the hypothesis that decreasing BDNF is the primary pathway by which IFN-a worsens depression. Nonetheless, the results support the hypothesis that BDNF levels influence resiliency against developing inflammatory cytokine-associated depression, and specifically to a subset of symptoms distinct from those influenced by 5-HTTLPR. Neuropsychopharmacology (2013) 38, 985-995;

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“…This interaction monitors the development and plasticity of the neural circuits which have a role in MDs. Likewise, antidepressant drugs can alter the levels of neurotrophic factors and therefore are able to contribute in neuronal plasticity [9] . Different parts of the brain are involved in the regulation of mood and the expression of emotions, as well as other functions, like reward processing [10] .…”

Section: Introductionmentioning

confidence: 99%

Mood disorders: A potential link between ghrelin and leptin on human body?

Zarouna

Wozniak

2015

WJEM

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Leptin and ghrelin are two hormones associated with multiple physiological functions, especially energy balance. Leptin is an adipocyte-secreted hormone discovered in 1950 and ghrelin which was found in 1999, is a peptide hormone produced and secreted in the stomach. A number of previous studies showed that these hormones could be associated with different types of mood disorders. The results of previous studies, nevertheless, are confounded by diverse sample selection and different methodologies. A search for related articles in the PubMed database was attempted. The search covered studies, reports, reviews and editorials published in the last ten years. Older references served as auxiliary sources for comparison purposes. However, due to the different results of the studies, there is a need for more investigation in order to establish the exact biochemical mechanisms that are responsible for these diseases and ghrelin's and leptin's effects on mood. Core tip: Mood disorders are affecting a major amount of the world population. Considering the multiple factors that are contributing in the development of mood disorders, this review emphasizes on the role of leptin and ghrelin hormones. These two hormones have a key role in energy balance but they also have an effect on other physiological functions too, therefore we emphasize on the recent findings which raise a potential link between the hormones and the disorders of mood.

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Neuronal plasticity: A link between stress and mood disorders

Cited by 260 publications

References 81 publications

Developmental Influence of the Serotonin Transporter on the Expression of Npas4 and GABAergic Markers: Modulation by Antidepressant Treatment

Developmental Influence of the Serotonin Transporter on the Expression of Npas4 and GABAergic Markers: Modulation by Antidepressant Treatment

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Mood disorders: A potential link between ghrelin and leptin on human body?

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