Glucocorticoid Hormones and Early Brain Development in Schizophrenia

Koenig, James I.; Kirkpatrick, M.D Brian; Lee, Paul

doi:10.1016/s0893-133x(01)00396-7

Cited by 181 publications

(38 citation statements)

References 125 publications

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“…Alcohol also causes brain volume loss in limbic areas which may be permanent (Rosenbloom et al, 2003), leaving open the possibility that a prior history of alcoholism could explain the findings. Finally, group differences in psychological stress or excessive HPAA activity could theoretically produce the structural changes (Koenig et al, 2002) though evidence indicates stress alters the medial, not lateral, hippocampus (Wang et al, 2010), and the effect of stress on hippocampal structure remains controversial.…”

Section: Discussionmentioning

confidence: 99%

Structural pathology underlying neuroendocrine dysfunction in schizophrenia

Goldman

Wang

Wachi

et al. 2011

Behavioural Brain Research

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Polydipsic hyponatremic schizophrenic (PHS) patients exhibit altered neuroendocrine activity that has been linked to their life-threatening water imbalance, as well as to impaired function and reduced volume of the anterior hippocampus. Polydipsic patients without hyponatremia (polydipsic normonatremic schizophrenics: PNS) exhibit similar, albeit less marked, changes in neuroendocrine activity and anterior hippocampal function, but not reduced anterior hippocampal volume. Indeed, reduced anterior hippocampal volume is seen in patients with normal water balance (nonpolydipsic normonatremic schizophrenics: NNS) whose neuroendocrine activity and anterior hippocampal function differ markedly from those with polydipsia. In an effort to reconcile these findings we measured hippocampal, amygdala and 3rd ventricle shapes in 26 schizophrenic patients (10 PNS, 7 PHS, 9 NNS) and 12 healthy controls matched for age and gender. Bilateral inward deformations were localized to the anterior lateral hippocampal surface (part of a neurocircuit which modulates neuroendocrine responses to psychological stimuli) in PHS and to a lesser extent in PNS, while deformations in NNS were restricted to the medial surface. Proportional deformations of the right medial amygdala, a key segment of this neurocircuit, were seen in both polydipsic groups, and correlated with the volume of the 3rd ventricle, which lies adjacent to the neuroendocrine nuclei. Finally, these structural findings were most marked in those with impaired hippocampal-mediated stress responses. These results reconcile previously conflicting data, and support the view that anterior lateral hippocampal pathology disrupts neuroendocrine function in polydipsic patients with and without hyponatremia. The relationship of these findings to the underlying mental illness remains to be established.

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Section: Discussionmentioning

confidence: 99%

Structural pathology underlying neuroendocrine dysfunction in schizophrenia

Goldman

Wang

Wachi

et al. 2011

Behavioural Brain Research

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“…The idea that GC excess early in life can reprogram HPA axis reactivity in part through decreasing GR expression in specific brain regions that are responsible for mediating negative feedback. In support of this concept, fetal GC excess in humans has been found to increase the risk for schizophrenia in adulthood (Koenig et al, 2002). Moreover increased fetal GCs due to maternal obesity or malnutrition also increases the risk of schizophrenia when the child grows into an adult (Khandaker et al, 2012; Lesage et al, 2001; Reynolds et al, 2013; Sasaki et al, 2013).…”

Section: Clinical Effects Of Impaired Gc Signalingmentioning

confidence: 92%

Dissection of glucocorticoid receptor-mediated inhibition of the hypothalamic–pituitary–adrenal axis by gene targeting in mice

Laryea

Muglia

Arnett

et al. 2015

Frontiers in Neuroendocrinology

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Negative feedback regulation of glucocorticoid (GC) synthesis and secretion occurs through the function of glucocorticoid receptor (GR) at sites in the hypothalamic-pituitary-adrenal (HPA) axis, as well as in brain regions such as the hippocampus, prefrontal cortex, and sympathetic nervous system. This function of GRs in negative feedback coordinates basal glucocorticoid secretion and stress-induced increases in secretion that integrate GC production with the magnitude and duration of the stressor. This review describes the effects of GR loss along major sites of negative feedback including the entire brain, the paraventricular nucleus of the hypothalamus (PVN), and the pituitary. In genetic mouse models, we evaluate circadian regulation of the HPA axis, stress-stimulated neuroendocrine response and behavioral activity, as well as the integrated response of organism metabolism. Our analysis provides information on contributions of region-specific GR-mediated negative feedback to provide insight in understanding HPA axis dysregulation and the pathogenesis of psychiatric and metabolic disorders.

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“…Maternal stress is weakly associated with an increased risk for neurodevelopmental disorders including schizophrenia, autism spectrum disorders and attention deficit disorders in humans (Brown 2012; Khashan et al 2008; Kinney et al 2008; Koenig et al 2002; Ronald et al 2010). Numerous studies have examined maternal stress and its direct effects on the developing fetus and have been reviewed elsewhere (Bagot et al 2014; Bowers and Yehuda 2016; Pena et al 2014).…”

Section: Intergenerational/transgenerational Transmission Of Stress Smentioning

confidence: 99%

Understanding the epigenetic basis of sex differences in depression

Hodes

Walker

Labonté

et al. 2016

J of Neuroscience Research

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Epigenetics refers to potentially heritable processes that can mediate both lasting and transient changes in gene expression in the absence of genome sequence alterations. The field of epigenetics has introduced a novel understanding of the mechanisms through which the environment can shape an individual and potentially its offspring. This review examines the current literature exploring the role of epigenetics in the development of mood disorders such as depression. Depression is ~2-fold more common in females, yet the majority of pre-clinical research has been conducted exclusively in male subjects. Here we discuss what is known about sex differences in epigenetic regulation and function and how this may contribute to the etiology and onset of mood disorders.

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Glucocorticoid Hormones and Early Brain Development in Schizophrenia

Cited by 181 publications

References 125 publications

Structural pathology underlying neuroendocrine dysfunction in schizophrenia

Structural pathology underlying neuroendocrine dysfunction in schizophrenia

Dissection of glucocorticoid receptor-mediated inhibition of the hypothalamic–pituitary–adrenal axis by gene targeting in mice

Understanding the epigenetic basis of sex differences in depression

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