Sleep deprivation and bright light as potential augmenters of antidepressant drug treatment—Neurobiological and psychometric assessment of course

Holsboer‐Trachsler, Edith; Hemmeter, Ulrich; Hatzinger, Martin; Seifritz, Erich; Gerhard, Urs; Hobi, V.

doi:10.1016/0022-3956(94)90020-5

Cited by 108 publications

(51 citation statements)

References 34 publications

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“…As a result, dysregulation of the HPA axis has been implicated in depression and its treatment. Clinical data indicates that a subset of patients with depression exhibit hyperactivity of the HPA axis, which is normalized after successful antidepressant therapy (Asnis et al, 1992;Holsboer-Trachsler et al, 1994;Gold et al, 1995;Heuser et al, 1996;Arborelius et al, 1999;Sapolsky, 2000).…”

Section: Discussionmentioning

confidence: 99%

Inducible cAMP Early Repressor Regulates Corticosterone Suppression after Tricyclic Antidepressant Treatment

et al. 2004

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The cAMP-response element binding protein (CREB) is involved in antidepressant action, but the role of related CRE-binding transcription factors in the behavioral and endocrine responses to antidepressants is unclear. Alternative transcription of the cAMP response element-modulator (CREM) gene yields activator and repressor isoforms, including the strong repressor inducible cAMP early repressor (ICER). ICER is highly expressed in hypothalamic tissues and upregulated after electroconvulsive seizure. Thus, ICER may be a novel mediator of antidepressant action at endocrine and/or behavioral levels. Here we establish that both subchronic and chronic desipramine (DMI) treatments upregulate hypothalamic ICER expression in wild-type mice. Behavioral responses to DMI in the forced swim and tail suspension tests are unchanged in mice lacking ICER. However, the ability of DMI to suppress an acute corticosterone response after swim stress is compromised in ICER-deficient mice, suggesting that increased hypothalamic ICER mRNA after DMI treatment may be required for suppression of corticosterone release. To investigate the mechanism underlying this response, we measured corticotropin releasing factor (CRF), an upstream modulator of corticosterone release. Using real-time quantitative PCR, we establish that hypothalamic CRF expression is significantly reduced after swim exposure in DMI-treated wild-type mice, however DMI is unable to blunt hypothalamic CRF expression in ICER-deficient mice. Furthermore, we demonstrate that ICER is enriched in CRF-expressing neurons in the paraventricular nucleus of the hypothalamus. These data indicate that ICER is required for DMI to reduce stress-induced corticosterone release through regulation of hypothalamic CRF expression, revealing a novel role for ICER in antidepressant regulation of the hypothalamic-pituitary adrenal axis.

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Section: Discussionmentioning

confidence: 99%

Inducible cAMP Early Repressor Regulates Corticosterone Suppression after Tricyclic Antidepressant Treatment

et al. 2004

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“…The combined dex/CRH test proved particularly useful as a predictor of increased risk for relapse (Holsboer et al 1987;Holsboer-Trachsler et al 1994;Heuser et al 1996;Zobel et al 1999).…”

Section: Functional Impairment Of Central Corticosteroid Receptors CLmentioning

confidence: 99%

“…Theoretically, mifepristone may be particularly effective in psychotic depression where the HPA system is most frequently hyperactive and where cortisol induced inhibition of dopamine metabolism may be involved in the pathogenesis of this subtype of depression (Schatzberg et al 1985). In fact, trimipramin, an effective antidepressant monotherapy of psychotic depression, suppresses hypersecretion of cortisol very effectively (Holsboer-Trachsler et al 1994;Sonntag et al 1996).…”

Section: Corticosteroid Receptor Antagonistsmentioning

confidence: 99%

The Corticosteroid Receptor Hypothesis of Depression

Holsboer

2000

Neuropsychopharmacology

1,978

1,228

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Clinical EvidenceUntil now, the serendipitous discovery of antidepressants in the 1950s has profoundly inspired hypotheses of the pathogenesis of depression. The well-known pharmacological effects of antidepressants on presynaptic uptake transporters and degradating enzymes (i.e., MAO) of serotonin and norepinephrine has focused research on causality and treatment of depression on the metabolism of functional biogenic amines and the capacity of their respective receptors to alter intracellular signaling pathways that ultimately induce changes in gene activity. Elevated circulating levels of stress hormones among depressives were recognized even before antidepressants were discovered, but these changes were seen as epiphenomena, reflecting the stressful experience of depression, although M. Bleuler (1919) already demonstrated that hormones have diverse psychotropic effects and suggested hormone treatments as potential antidepressants. A vast amount of evidence has accumulated, that reject the view that altered stress hormone secretions in depression are epiphenomenal. During the past decade, several research groups formulated a hypothesis relating aberrant stress hormone dysregulation to causality of depression and submitted that antidepressants may act through normalisation of these HPA changes (

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“…32,58 Further, the combination of light regimens with antidepressant compounds such as imipramine, sertraline, and citalopram has been shown to significantly improve mood, with faster response rates than an antidepressant-only control group. [59][60][61][62][63] In addition, melatonin levels have also been found to show significant differences in patients with nonseasonal major depression when compared with healthy individuals. 64 Due to the very nature of nonseasonal depression and its multifactorial causes and symptoms, a purely chronobiological light-driven treatment regime would be difficult to apply.…”

Section: Nonseasonal Depressionmentioning

confidence: 99%

An insight into light as a chronobiological therapy in affective disorders

Walsh¹,

Atkinson²,

Corlett³

et al. 2014

CPT

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Abstract:The field of chronobiology has vastly expanded over the past few decades, bringing together research from the fields of circadian rhythms and sleep. The importance of the environmental day-night cycle on our health is becoming increasingly evident as we evolve into a 24-hour society. Reducing or changing sleep times against our natural instincts to rest at night has a detrimental impact on our well-being. The mammalian circadian clock, termed "the suprachiasmatic nucleus", is responsible for synchronizing our behavioral and physiological outputs to the environment. It utilizes light transcoded by specialized retinal photoreceptors as its cue to set internal rhythms to be in phase with the light-dark cycle. Misalignment of these outputs results in symptoms such as altered/disturbed sleep patterns, changes in mood, and physical and mental exhaustion -symptoms shared by many affective clinical disorders. Key links to circadian abnormalities have been found in a number of disorders, such as seasonal affective disorder, nonseasonal depression, and bipolar affective disorder. Furthermore, therapies developed through chronobiological research have been shown to be beneficial in the treatment of these conditions. In this article, we discuss the impact of circadian research on the management of affective disorders, giving evidence of how a misaligned circadian system may be a contributor to the symptoms of depression and how moderating circadian rhythms with light therapy benefits patients.

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Sleep deprivation and bright light as potential augmenters of antidepressant drug treatment—Neurobiological and psychometric assessment of course

Cited by 108 publications

References 34 publications

Inducible cAMP Early Repressor Regulates Corticosterone Suppression after Tricyclic Antidepressant Treatment

Inducible cAMP Early Repressor Regulates Corticosterone Suppression after Tricyclic Antidepressant Treatment

The Corticosteroid Receptor Hypothesis of Depression

An insight into light as a chronobiological therapy in affective disorders

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