Divergent endocrine abnormalities in melancholic and atypical depression: clinical and pathophysiologic implications

Gold, Philip W.; Gabry, K. Eddie; Yasuda, Mariko; Chrousos, George P.

doi:10.1016/s0889-8529(01)00022-6

Cited by 123 publications

(101 citation statements)

References 105 publications

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“…Whether stress influences hippocampal function and structure is an important question to human health for several reasons. First, correlational and epidemiological studies have implicated stress in human disorders that involve the hippocampus, including dementia, 60,61 depression, 62,63 and schizophrenia. 13 In addition, genetic predisposition accounts for only a fraction of diseases -such as Alzheimer's -where hippocampal dysfunction is profound.…”

Section: Discussionmentioning

confidence: 99%

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent

et al. 2006

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The effects of stress, including their putative contribution to pathological psychiatric conditions, are crucially governed by the age at which the stress takes place. However, the cellular and molecular foundations for the impact of stress on neuronal function, and their change with age, are unknown. For example, it is not known whether 'psychological' stress signals are perceived by similar neuronal populations at different ages, and whether they activate similar or age-specific signaling pathways that might then mediate the spectrum of stress-evoked neuronal changes. We employed restraint and restraint/noise stress to address these issues in juvenile (postnatal day 18, [P18]) and adult rats, and used phosphorylation of the transcription factor CREB (pCREB) and induction of c-fos as markers of hippocampal neuronal responses. Stress-activated neuronal populations were identified both anatomically and biochemically, and selective blockers of the stress-activated hippocampal peptide, corticotropin-releasing hormone (CRH) were used to probe the role of this molecule in stressinduced hippocampal cell activation. Stress evoked strikingly different neuronal response patterns in immature vs adult hippocampus. Expression of pCREB appeared within minutes in hippocampal CA3 pyramidal cells of P18 rats, followed by delayed induction of Fos protein in the same cell population. In contrast, basal pCREB levels were high in adult hippocampus and were not altered at 10-120 min by stress. Whereas Fos induction was elicited by stress in the adult, it was essentially confined to area CA1, with little induction in CA3. At both age groups, central pretreatment with either a nonselective blocker of CRH receptors or the CRF 1 -selective antagonist, NBI 30775, abolished stress-evoked neuronal activation. In conclusion, hippocampal neuronal responses to psychological stress are generally more rapid and robust in juvenile rats, compared to fully mature adults, and at both ages, CRH plays a key role in this process. Enhanced hippocampal response to stress during development, and particularly the activation of the transcription factor CREB, may contribute to the enduring effects of stress during this period on hippocampal function.

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Section: Discussionmentioning

confidence: 99%

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent

et al. 2006

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“…Consistent with these studies, the inability of the HPA axis to respond to stressors and to maintain homeostatic regulation is a robust biological fi nding in MDD and PPD. This inability is due to the impaired negative feedback mediated by cortisol receptors in the anterior pituitary, hypothalamus, and hippocampus, as well as ACTH (adrenocortical hormone) receptors in the anterior pituitary and CRH autoreceptors in the hypothalamus [5,33,34] . Women with PPD and non-puerperal women with MDD display similar abnormalities in HPA axis activity and exhibit high baseline cortisol levels and exaggerated responses to the dexamethasone/CRH test.…”

Section: Perinatal Depression and The Hpa Axismentioning

confidence: 99%

“…In the same context, euthymic women with a past history of PPD who undergo a protocol consisting of high-dose gonadal steroid administration followed by abrupt withdrawal exhibit an increased cortisol response and onset of signifi cant depressive symptoms compared to normal women. Such results posit that a vulnerability trait related to the onset of PPD does exist or may develop as a consequence of a previous depression [34] . …”

mentioning

confidence: 93%

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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Abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis is an important pathological finding in pregnant women exhibiting major depressive disorder. They show high levels of cortisol proinflammatory cytokines, hypothalamic-pituitary peptide hormones and catecholamines, along with low dehydroepiandrosterone levels in plasma. During pregnancy, the TH2 balance together with the immune system and placental factors play crucial roles in the development of the fetal allograft to full term. These factors, when altered, may generate a persistent dysfunction of the HPA axis that may lead to an overt transfer of cortisol and toxicity to the fetus at the expense of reduced activity of placental 11β-hydroxysteroid dehydrogenase type 2. Epigenetic modifications also may contribute to the dysregulation of the HPA axis. Affective disorders in pregnant women should be taken seriously, and therapies focused on preventing the deleterious effects of stressors should be implemented to promote the welfare of both mother and baby.Keywords: brain; depression; neuroendocrine; pregnancy; stress; glucocorticoids Extensive studies have demonstrated that early life stressors produce changes in behavior and enhance the sensitivity of the stress response systems [1][2][3][4] . Although the genetic background has been implicated in the development of mood-related disorders, and genetic research has identified some chromosomal regions and genes that are involved in susceptibility to mood disorders, the etiology of anxiety and depressive disorders is still not clear in humans, particularly in women with major depressive disorder (MDD) [1] .The pathogenesis of perinatal depression is an emerging field. Although considerable progress has been made in this area in the last few years, there still remain unanswered questions and gaps in our knowledge of the underlying pathogenesis, the long-term impact of perinatal depression on the developing fetus, and the best methods for counseling pregnant women concerning the risks of untreated MDD versus the risks of psychopharmacologic treatment during pregnancy and lactation [5] . Meta-analysis studies have reported that the mean prevalence rate of prenatal depression is ~12% (this varies greatly according to location, mode of assessment, and socioeconomic conditions), and show that a large percentage of pregnant women displaying major depression remain depressed in the postpartum period and/or continuously [6,7] . Anxiety, depressive disorder, and stress during pregnancy are risk Phillipe Leff Gelman, et al. HPA axis in perinatal depression 339 factors for negative outcomes in newborns, like preterm birth or low birth weight; also, insecure attachment and impaired child development could be a consequence of mental disorders during pregnancy [6,[8][9][10] . The mechanisms by which maternal depression impacts fetal and neonatal development are currently under investigation; there is some evidence that depressive symptoms impact the infant's hypothalamic-pituitary-adrenal (HPA) axis, enhancing the ...

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“…This response, involving the release of mediators of allostasis (e.g. adrenal hormones, neurotransmitters, and cytokines (see Table 2)), works via receptors in various tissues and organs to produce changes that are adaptive to metabolism, immune, and cardiovascular systems in the short term [11,13,14,17,22,29,30].…”

Section: Allostasis Allostatic State and Allostatic Loadmentioning

confidence: 99%

A new animal welfare concept based on allostasis

Korte

Olivier

Koolhaas

2007

Physiology & Behavior

258

181

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Animal welfare is an increasing issue of public concern and debate. As a result, many countries are reconsidering the way animal welfare is embedded in the legislation and rules for housing and care of animals. This requires general agreement of what animal welfare is. Unfortunately, the current science of animal welfare is less scientific than what has been claimed. In our view, it is overly guided by anthropocentric thinking about how animals ought to be handled and neglects the latest concept of physiology: 'The Allostasis Concept'. Allostasis, which means stability through change, has the potential to replace homeostasis as the core model of physiological regulation. Not constancy or freedoms, but capacity to change is crucial to good physical and mental health and good animal welfare. Therefore, not homeostasis but allostasis is at the basis of our new animal welfare concept. This paper is aimed at a broader scientific discussion of animal welfare that includes knowledge from the latest scientific developments in neurobiology and behavioral physiology, and generates views that are extremely relevant for the animal welfare discussion.

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Divergent endocrine abnormalities in melancholic and atypical depression: clinical and pathophysiologic implications

Cited by 123 publications

References 105 publications

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent

Hypothalamic-pituitary-adrenal axis function during perinatal depression

A new animal welfare concept based on allostasis

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