Neuronal actions of glucocorticoids: Focus on depression

Yu, Sheng-Bo; Holsboer, Florian; Almeida, Osborne F. X.

doi:10.1016/j.jsbmb.2007.09.014

Cited by 72 publications

(50 citation statements)

References 101 publications

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“…In turn, the dysregulation of the HPA axis has been regarded as a neuroendocrine hallmark of chronic stress [45,46] and (in a form of either DEX suppression or the combined DEX/CRH tests) has been used as a diagnostic tool in depression [47]. Mechanisms by which the dysregulated HPA axis leads to depression are apparently multiple.…”

Section: Il-1ra Monotherapymentioning

confidence: 99%

Interleukin-1beta Causes Fluoxetine Resistance in an Animal Model of Epilepsy-Associated Depression

et al. 2012

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Depression represents a common comorbidity of epilepsy and is frequently resistant to selective serotonin reuptake inhibitors (SSRI). We tested the hypothesis that the SSRI resistance in epilepsy associated depression may be a result of a pathologically enhanced interleukin-1β (IL1-β) signaling, and consequently that the blockade of IL1-β may restore the effectiveness of SSRI. Epilepsy and concurrent depression-like impairments were induced in Wistar rats by pilocarpine status epilepticus (SE). The effects of the 2-week long treatment with fluoxetine, interleukin-1 receptor antagonist (IL-1ra), and their combination were examined using behavioral, biochemical, neuroendocrine, and autoradiographic assays. In post-SE rats, depression-like impairments included behavioral deficits indicative of hopelessness and anhedonia; the hyperactivity of the hypothalamo-pituitaryadrenocortical axis; the diminished serotonin output from raphe nucleus; and the upregulation of presynaptic serotonin 1-A (5-HT1A) receptors. Fluoxetine monotherapy exerted no antidepressant effects, whereas the treatment with IL-1ra led to the complete reversal of anhedonia and to a partial improvement of all other depressive impairments. Combined administration of fluoxetine and IL-1ra completely abolished all hallmarks of epilepsy-associated depressive abnormalities, with the exception of the hyperactivity of the hypothalamopituitary-adrenocortical axis, the latter remaining only partially improved. We propose that in certain forms of depression, including but not limited to depression associated with epilepsy, the resistance to SSRI may be driven by the pathologically enhanced interleukin-1β signaling and by the subsequent upregulation of presynaptic 5-HT1A receptors. In such forms of depression, the use of interleukin-1β blockers in conjunction with SSRI may represent an effective therapeutic approach.

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Section: Il-1ra Monotherapymentioning

confidence: 99%

Interleukin-1beta Causes Fluoxetine Resistance in an Animal Model of Epilepsy-Associated Depression

et al. 2012

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“…HPA-A dysregulation involves a failure of autoinhibitory mechanisms via which circulating cortisol (or corticosterone in rodents) inhibits the release of corticotropin releasing hormone (CRH) from the hypothalamus and of adrenocorticotropic hormone (ACTH) from anterior pituitary. In turn, unabated production of CRH and ACTH lead to high sustained levels of circulating cortisol [106][107][108]. Consequently, the function of the HPA-A switches from adaptive (i.e., to effectively cope with stressful stimuli) to maladaptive.…”

Section: Dysregulation Of the Hpa-amentioning

confidence: 99%

“…Experimental evidence that the hyperactivity of the HPA-A leads to depressive behavior is overwhelming [107][108][109][110][111][112]. Thus, chronic stress induced in rodents by maternal separation, prolonged physical restrain, cold stress, and sleep deprivation results in the HPA-A hyperactivity [112][113][114][115]; the latter is evident by the elevated plasma corticosterone level and/or positive DEX or DEX/CRH tests [116].…”

Section: Dysregulation Of the Hpa-amentioning

confidence: 99%

Biomarkers of Epileptogenesis: Psychiatric Comorbidities (?)

Kanner

Mazarati

Koepp³

2014

Neurotherapeutics

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The last decade has witnessed a significant shift on our understanding of the relationship between psychiatric disorders and epilepsy. While traditionally psychiatric disorders were considered as a complication of the underlying seizure disorder, new epidemiologic data, supported by clinical and experimental research, have suggested the existence of a bidirectional relation between the two types of conditions: not only are patients with epilepsy at greater risk of experiencing a psychiatric disorder, but patients with primary psychiatric disorders are at greater risk of developing epilepsy. Do these data suggest that some of the pathogenic mechanisms operant in psychiatric comorbidities play a role in epileptogenesis? The aim of this article is to review the epidemiologic data that demonstrate that primary psychiatric disorders are more frequent in people who develop epilepsy, before the onset of the seizure disorder than among controls. The next question looks at the available data of pathogenic mechanisms of primary mood disorders and their potential for facilitating the development and/or exacerbation in the severity of epileptic seizures. Finally, we review data derived from experimental studies in animal models of depression and epilepsy that support a potential role of pathogenic mechanisms of mood disorders in the development of epileptic seizures and epileptogenesis. The data presented in this article do not yet establish conclusive evidence of a pathogenic role of psychiatric comorbidities in epileptogenesis, but raise important research questions that need to be investigated in experimental, clinical, and population-based epidemiologic research studies.

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“…If cortical hedonic signals decrease by applying a pre-established hypocaloric diet, the increase of serotonin signalling helps reduce body weight (dexfenfluramine, sibutramine) 263,264 in a process akin to the treatment of depression (fluoxetine, sertraline). 265,266 Again, glucocorticoids counter these effects and induce depression, 267 which may be counteracted by serotonergic stimulation. 268 The implication of cannabinoid receptors 269 (rimonabant is an inverse cannabinoid CB1receptor blocker 270 ), and catecholamines (amphetamine inhibiting food intake 271 and phentermine or ephedrine increasing energy expenditure 272 ) shows that the mechanisms controlling food intake and energy output, i.e.…”

Section: Other Aspects Of the Brain -Adipose Tissue Interactionmentioning

confidence: 99%

Steroid hormones interrelationships in the metabolic syndrome: An introduction to the ponderostat hypothesis

Alemany¹

2012

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Neuronal actions of glucocorticoids: Focus on depression

Cited by 72 publications

References 101 publications

Interleukin-1beta Causes Fluoxetine Resistance in an Animal Model of Epilepsy-Associated Depression

Interleukin-1beta Causes Fluoxetine Resistance in an Animal Model of Epilepsy-Associated Depression

Biomarkers of Epileptogenesis: Psychiatric Comorbidities (?)

Steroid hormones interrelationships in the metabolic syndrome: An introduction to the ponderostat hypothesis

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