Stress-induced activation of the brainstem Bcl-xL gene expression in rats treated with fluoxetine: Correlations with serotonin metabolism and depressive-like behavior

Шишкина, Г. Т.; Kalinina, Tatyana; Berezova, I. V.; Дыгало, Н. Н.

doi:10.1016/j.neuropharm.2011.06.016

Cited by 30 publications

(23 citation statements)

References 66 publications

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“…Although the mechanisms by which GRs may be implicated in an antidepressant-like effect of DEX remain to be determined, it is possible that the ability of glucocorticoids to increase expression of anti-apoptotic proteins (Gascoyne et al 2003;Viegas et al 2004) plays a role in the generation of DEX-induced behavior. This suggestion is consistent with the previous studies showing the involvement of anti-apoptotic proteins in the emotional consequences of stress McKernan et al 2009;Shishkina et al 2010Shishkina et al , 2012Wann et al 2007). After acute corticosterone treatment, GRs and anti-apoptotic proteins were shown to form complexes which translocate into mitochondria and enhance active coping mechanisms in response to aversive or stressful stimuli (Du et al 2009).…”

Section: Discussionsupporting

confidence: 94%

Behavioral effects of glucocorticoids during the first exposures to the forced swim stress

2014

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Section: Discussionsupporting

confidence: 94%

Behavioral effects of glucocorticoids during the first exposures to the forced swim stress

2014

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“…Stress-induced activation of this gene expression appeared concomitantly with the anti-depressant-like effect during the course of fluoxetine treatment. This fact, together with the significant negative correlation between Bcl-xL mRNA levels in the brainstem and duration of immobility in the forced swim test (Shishkina et al 2012) implicate Bcl-xL in the mechanisms through which anti-depressant drugs facilitate coping responses to external stimuli.…”

Section: Expression Of Neuroplasticity and Serotonergic Markers In Thmentioning

confidence: 93%

“…Robust anti-depressant-like effects of SSRIs occur after long-term drug treatment (Fuller 1995). For example, immobility was significantly decreased by administration of fluoxetine for 4 and 8 weeks, whereas the decrease after fluoxetine for 2 weeks did not reach statistical significance (Shishkina et al 2012). …”

Section: Expression Of Neuroplasticity and Serotonergic Markers In Thmentioning

confidence: 98%

“…Changes in the expression of genes related to the activity of 5-HT system [tryptophan hydroxylase-2 (TPH2), the rate-limiting enzyme in the biosynthesis of 5-HT specifically in the brain, 5-HT transporter (5-HTT) that mediates reuptake of extracellular 5-HT and 5-HT1A receptors, which in the raphe nuclei regulate the firing rate of 5-HT neurons] and neuronal plasticity (BDNF, Bcl-xL, and Bax) in the brainstem of rats treated with fluoxetine and exposed to forced swim stress support involvement of this brain region in the mechanisms of mood-related behaviors (Shishkina et al 2012). In this study, immobility duration in the forced swim test was also used as an index of depression-like state in rodents (Cryan et al 2005).…”

Section: Expression Of Neuroplasticity and Serotonergic Markers In Thmentioning

confidence: 99%

“…Several apoptotic proteins, namely caspase-3, proapoptotic Bcl-xL/Bcl-2-associated death promoter (Bad) and Bcl-2-associated X (Bax) proteins, have been implicated in the development of NMDA receptor-dependent long-term depression of synaptic transmission that could be prevented by overexpression of Bcl-xL Jiao and Li 2011). Recent studies have found a close association of this antiapoptotic protein expression in brain regions with individual differences in behavioral vulnerability to short-lasting stress (Shishkina et al 2010) as well as with the behavioral response to chronic anti-depressant treatment (Shishkina et al 2012). These findings are discussed in the context of the role of BclxL in the mechanisms of individual differences in behavioral resilience to stress and anti-depressant effects.…”

Section: Introductionmentioning

confidence: 99%

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Increased Expression of the Anti-Apoptotic Protein Bcl-xL in the Brain is Associated with Resilience to Stress-Induced Depression-Like Behavior

et al. 2012

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Clinical observations and the results of animal studies have implicated changes in neuronal survival and plasticity in both the etiology of mood disorders, especially stress-induced depression, and anti-depressant drug action. Stress may predispose individuals toward depression through down-regulation of neurogenesis and an increase in apoptosis in the brain. Substantial individual differences in vulnerability to stress are evident in humans and were found in experimental animals. Recent studies revealed an association between the brain anti-apoptotic protein B cell lymphoma like X, long variant (Bcl-xL) expression and individual differences in behavioral vulnerability to stress. The ability to increase Bcl-xL gene expression in the hippocampus in response to stress may be an important factor for determining the resistance to the development of stress-induced depression. Treatment with anti-depressant drugs may change Bcl-xL response properties. In the rat brainstem, expression of this anti-apoptotic gene becomes sensitive to swim stress during the long-term fluoxetine treatment, an effect that appeared concomitantly with the anti-depressant-like action of the drug in the forced swim test, suggesting that Bcl-xL may be a new target for depression therapy. The processes and pathways linking stress stimuli to behavior via intracellular anti-apoptotic protein are discussed here in the context of Bcl-xL functions in the mechanisms of individual differences in behavioral resilience to stress and anti-depressant-induced effects on the behavioral despair.

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Advances in tryptophan hydroxylase‐2 gene expression regulation: New insights into serotonin–stress interaction and clinical implications

Chen

Miller

2012

American J of Med Genetics Pt B

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Serotonin (5-HT) modulates the stress response by interacting with the hormonal hypothalamic-pituitary-adrenal (HPA) axis and neuronal sympathetic nervous system (SNS). Tryptophan hydroxylase (TPH) is the rate-limiting enzyme in 5-HT biosynthesis, and the recent identification of a second, neuron-specific TPH isoform (TPH2) opened up a new area of research. While TPH2 genetic variance has been linked to numerous behavioral traits and disorders, findings on TPH2 gene expression have not only reinforced, but also provided new insights into, the long-recognized but not yet fully understood 5-HT-stress interaction. In this review, we summarize advances in TPH2 expression regulation and its relevance to the stress response and clinical implications. Particularly, based on findings on rhesus monkey TPH2 genetics and other relevant literature, we propose that: 1) upon activation of adrenal cortisol secretion, the cortisol surge induces TPH2 expression and de novo 5-HT synthesis; 2) the induced 5-HT in turn inhibits cortisol secretion by modulating the adrenal sensitivity to ACTH via the suprachiasmatic nuclei (SCN)-SNS-adrenal system, such that it contributes to the feedback inhibition of cortisol production; 3) basal TPH2 expression or 5-HT synthesis, as well as early-life experience, influence basal cortisol primarily via the hormonal HPA axis; and 4) 5′- and 3′-regulatory polymorphisms of TPH2 may differentially influence the stress response, presumably due to their differential roles in gene expression regulation. Our increasing knowledge of TPH2 expression regulation not only helps us better understand the 5-HT-stress interaction and the pathophysiology of neuropsychiatric disorders, but also provides new strategies for the treatment of stress-associated diseases.

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Stress-induced activation of the brainstem Bcl-xL gene expression in rats treated with fluoxetine: Correlations with serotonin metabolism and depressive-like behavior

Cited by 30 publications

References 66 publications

Behavioral effects of glucocorticoids during the first exposures to the forced swim stress

Behavioral effects of glucocorticoids during the first exposures to the forced swim stress

Increased Expression of the Anti-Apoptotic Protein Bcl-xL in the Brain is Associated with Resilience to Stress-Induced Depression-Like Behavior

Advances in tryptophan hydroxylase‐2 gene expression regulation: New insights into serotonin–stress interaction and clinical implications

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