Glucocorticoid receptor number and cortisol excretion in mood, anxiety, and psychotic disorders

Yehuda, Rachel; Boisoneau, David; Mason, John W.; Giller, Earl L.

doi:10.1016/0006-3223(93)90252-9

Cited by 241 publications

(127 citation statements)

References 28 publications

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“…Our finding of a lower leukocyte GR density is in contrast with other studies that reported higher leukocyte GR density in PTSD compared to healthy controls 28,29 or data by the same group suggesting that there are no differences in GR density between PTSD patients and trauma or healthy controls. [29][30][31] Differences in the method used to assess GR density may have contributed to the discrepancy in results between GR binding studies.…”

Section: Discussioncontrasting

confidence: 99%

“…In addition, these measurements have been used as an easily accessible model to investigate glucocorticoid regulation of the HPA axis in previous studies. [28][29][30] However, contradicting data exist as to whether glucocorticoid sensitivity is a characteristic of the individual, for example GR polymorphisms, or is dependent on the target tissue investigated. Some studies described similar regulation of GR in the brain and in the immune system 41,42 whereas other studies did not observe correlation in GR sensitivity between different target tissues.…”

Section: Discussionmentioning

confidence: 99%

“…The immune modulating effect of glucocorticoids not only depends on the level of circulating cortisol but also on the number and subtypes of GRs in immune cells and on molecular interactions downstream of receptor activation. 27 Some early studies that assessed peripheral blood mononuclear cell (PBMC) GR density and binding affinity in PTSD report higher PBMC GR density in PTSD, 28,29 but later studies did not replicate these findings. [30][31][32] Flow cytometric determination of GR expression in lymphocyte subpopulations even revealed a lower GR expression in all lymphocyte subsets from PTSD patients compared to healthy individuals.…”

Section: Introductionmentioning

confidence: 99%

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Leukocyte glucocorticoid receptor expression and immunoregulation in veterans with and without post-traumatic stress disorder

et al. 2007

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Post-traumatic stress disorder (PTSD) is associated with a dysregulation of the hypothalamus-pituitary-adrenal axis (HPA axis). In addition, there is evidence for altered glucocorticoid receptor (GR) expression and function in peripheral blood mononuclear cells. The aim of the present study was to differentiate between the effect of trauma exposure and PTSD on leukocyte GR expression and glucocorticoid immune regulation. Leukocyte GR binding characteristics and glucocorticoid sensitivity of immune activity, determined as the effect of dexamethasone (DEX) on in vitro cytokine release and T-cell proliferation, were compared between veterans with PTSD, traumatized veterans without PTSD and healthy controls. Leukocyte GR density was significantly lower in veterans with and without PTSD compared to healthy controls. DEX-induced inhibition of T-cell proliferation was significantly lower in PTSD compared to trauma and healthy controls. DEX-induced increase in lipopolysaccharidestimulated interleukin-10 was less pronounced in traumatized veterans with and without PTSD compared to healthy controls. No group differences were observed in the effect of DEX on other cytokines or in baseline immune activity, except for lower tumor necrosis factor-a production in PTSD patients compared to healthy controls. The results suggest that trauma exposure is sufficient to induce changes in GR binding characteristics, whereas resistance of T-cell proliferation to DEX only occurs in PTSD. DEX resistance of in vitro immune activity was not a general phenomenon, but was restricted to specific immune functions.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Leukocyte glucocorticoid receptor expression and immunoregulation in veterans with and without post-traumatic stress disorder

et al. 2007

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“…Interestingly, it has recently been reported that patients with bipolar disorder have decreased CAMKII in the prefrontal cortex at postmortem (Xing et al, 2002). Although data on cortisol levels were not available, it is established that this group of patients is at high risk of cortisol abnormalities of the type modelled here (Cervantes et al, 2001;Yehuda et al, 1993).…”

Section: Relevance To Aging and Depressionmentioning

confidence: 80%

Flattening the Glucocorticoid Rhythm causes Changes in Hippocampal Expression of Messenger RNAs Coding Structural and Functional Proteins: Implications for Aging and Depression

Gartside

Leitch

McQuade

et al. 2002

Neuropsychopharmacol

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Subtle changes in glucocorticoid levels, including a flattening of the diurnal rhythm with raised nadir, are prevalent, being characteristic of both aging and major depression. Both these conditions are also associated with deficits in hippocampally mediated cognitive functions. We hypothesized that this profile of glucocorticoid levels causes structural and functional changes in the hippocampus, which in turn may engender cognitive deficits. We implanted slow-release corticosterone pellets into adrenally intact adult male rats to produce a flattened glucocorticoid rhythm with levels clamped midway between the normal nadir and zenith. Using density profile analysis we measured hippocampal expression of messenger RNAs encoding structural and functional proteins. In rats with a flattened glucocorticoid rhythm, the expression of the mRNA coding for microtubule associated protein-2b (MAP2b) was reduced in CA3 relative to sham-operated controls, but unchanged in dentate gyrus and CA1. In contrast, the expression of the mRNA coding the alpha subunit of calciumcalmodulin dependent kinase (CAMKIIa) was reduced in dentate gyrus in animals with a flattened glucocorticoid rhythm, but unchanged in CA3. The expression of the mRNA coding the synaptic vesicle protein synaptophysin was unchanged in both CA3 and dentate gyrus. The data indicate that a flattening of the normal diurnal glucocorticoid rhythm decreases the hippocampal expression of mRNAs coding key structural and functional proteins, and does so in a regionally selective manner. The data may have relevance for cognitive deficits characteristic of aging and depression.

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“…Although technical aspects of sample collection (arterialized vs. nonarterialized) and norepinephrine metabolism (Murburg 1994) could account for some discrepancies, stress studies in normals report good correspondence between epinephrine and norepinephrine responses (Richter et al 1996), which is yet to be demonstrated in PTSD. HPA axis findings have been more consistent, with evidence of lower 24-hour cortisol secretion (Yehuda et al 1990), hypersensitive glucocorticoid negative feedback (Yehuda et al 1993b), and higher numbers of lymphocyte glucocorticoid receptors (Yehuda et al 1993a). However, others have reported elevated 24-hour cortisol secretion .…”

mentioning

confidence: 96%

Neuroendocrine and Psychophysiologic Responses in PTSD: A Symptom Provocation Study

Liberzon

Abelson

Flagel

et al. 1999

Neuropsychopharmacology

252

142

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Glucocorticoid receptor number and cortisol excretion in mood, anxiety, and psychotic disorders

Cited by 241 publications

References 28 publications

Leukocyte glucocorticoid receptor expression and immunoregulation in veterans with and without post-traumatic stress disorder

Leukocyte glucocorticoid receptor expression and immunoregulation in veterans with and without post-traumatic stress disorder

Flattening the Glucocorticoid Rhythm causes Changes in Hippocampal Expression of Messenger RNAs Coding Structural and Functional Proteins: Implications for Aging and Depression

Neuroendocrine and Psychophysiologic Responses in PTSD: A Symptom Provocation Study

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