Hypothalamic‐pituitary‐adrenocortical function in mixed and pure mania

Swann, Alan C.; Stokes, Peter E.; Casper, Regina C.; Secunda, Steven K.; Bowden, Charles L.; Berman, Nancy; Katz, Martin Μ.; Robins, Eli

doi:10.1111/j.1600-0447.1992.tb01468.x

Cited by 87 publications

(43 citation statements)

References 26 publications

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“…10,11,15,18 We present molecular evidence for a reduction (either statistically significant or trending toward significance) in the amplitudes (for BMAL1, REV-ERBa and DBP) and in the overall levels (for DEC2 and DBP) of circadian gene expression in fibroblasts from bipolar patients. BMAL1, the key transcription factor heterodimerizing with CLOCK or NPAS2, drives circadian expression of other clock genes and the clockcontrolled genes.…”

Section: Discussionmentioning

confidence: 79%

“…[5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][80][81][82] However, molecular evidence for altered circadian clock in bipolar disorder is still lacking. It has been reported that similar components of the clock machinery underlie rhythmic gene expression in cultured fibroblasts as in the central clock in the SCN.…”

Section: Discussionmentioning

confidence: 99%

“…In bipolar patients, alterations in phase, period and amplitude of circadian rhythms have been documented by measuring core temperature, hormonal secretion or actigraphy. [8][9][10][11][12][13][14][15][16][17][18][19][20][21] In addition, lithium, the most effective treatment for bipolar disorder 22,23 lengthens the circadian period in mammalian cells [24][25][26] and in model organisms. [27][28][29] Lithium treatment of 293T cells leads to rapid proteosomal degradation of REV-ERBa and transcriptional activation of BMAL1, 30 which are critical components of core clock mechanism.…”

Section: Introductionmentioning

confidence: 99%

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Assessment of circadian function in fibroblasts of patients with bipolar disorder

et al. 2008

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Previous studies have implicated the circadian system in the pathophysiology of bipolar disorder, but conclusive evidence for altered circadian clocks is lacking. Cultured fibroblasts harbor circadian clocks representative of those in the master clock resident in the suprachiasmatic nuclei, providing a new avenue to investigate the core clock machinery in patients with bipolar illness. We examined the rhythmic expression patterns of core clock genes (BMAL1, PER1, PER2, REV-ERBa, DEC2, DBP) in fibroblasts from 12 bipolar patients and 12 healthy controls. Although we did not detect differences in the circadian period between bipolar patients and controls, the amplitude of rhythmic expression for BMAL1, REVERBa and DBP, as well as the overall mRNA expression level for DEC2 and DBP was reduced in fibroblasts from bipolar patients. Bonferroni's correction for multiple comparisons still resulted in significantly reduced DBP expression level, and trends toward reduced overall expression level of DEC2 and circadian amplitude of BMAL1, in fibroblasts from bipolar patients. We next examined an expanded cohort of 18 bipolar patients and 35 healthy controls for mRNA expression levels of four kinases (CKId, CKIe, GSK3a and GSK3b) and the protein and phosphorylation levels of two of them (GSK3a and GSK3b). We did not detect differences in steady-state mRNA levels or protein levels of these kinases between bipolar patients and controls, but the level of GSK3b phosphorylation was significantly reduced in bipolar patients within an Old Order Amish bipolar kindred. Our results suggest that the reduced amplitudes and overall expression levels of circadian genes, and the decreased phosphorylation level of GSK3b may lead to dysregulation of downstream genes, which could explain some pathological features of bipolar disorder.

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Section: Discussionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Assessment of circadian function in fibroblasts of patients with bipolar disorder

et al. 2008

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“…Mania with depressive features is more responsive to divalproex than to lithium (Swann et al 1997). A high state of arousal, possibly manifested neurochemically by increased catecholaminergic and hypothalamic-pituitary-adrenocortical function (Swann et al 1992) and behaviorally by irritability, depression, or anger (Swann et al 1986), may reduce the effectiveness of lithium in manic episodes. Identification of fundamental behavioral subtypes that differentially predict response to specific treatments could guide treatment choice.…”

mentioning

confidence: 99%

Pattern of Response to Divalproex, Lithium, or Placebo in Four Naturalistic Subtypes of Mania

Swann

Bowden

Calabrese

et al. 2002

Neuropsychopharmacology

124

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“…Cortisol may therefore be used as a biological marker of BD. Serotonin increases cortisol release by stimulating 5-HT 1A and 5-HT 2A receptors in hippocampal areas (Nurnberger et al 1990;Swann et al 1992;Vieta et al 1999). Changes in cortisol following challenge with selective 5-HT stimulating agents are possible biological markers to assess brain 5-HT function (Abel and Cleare 1999;Cleare et al 1998).…”

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confidence: 99%

Effects of Acute Tryptophan Depletion on Mood and Cortisol Release in First-degree Relatives of Type I and Type II Bipolar Patients and Healthy Matched Controls

Sobczak

Honig

Nicolson

et al. 2002

Neuropsychopharmacology

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Biological vulnerability for bipolar disorders (BD) in relatives of BD patients has not as yet been established. Serotonergic vulnerability was studied, using acute tryptophan depletion (ATD), in healthy first-degree relatives of BD patients and healthy controls. The effects of ATD on mood and cortisol release in 30 healthy adult, lifetime symptom free, unaffected first-degree relatives of BD patients (Family History; FH) were compared with effects in 15 healthy matched controls in a placebocontrolled, double-blind, crossover design. During ATD and placebo, salivary cortisol response was also assessed during a stress-inducing speech task (SIST). First-degree relatives of type II BD patients (FH II) showed an elevation of mood, whereas control subjects and relatives of type I BD patients (FH I) showed a lowering of mood after ATD. ATD was followed by a decrease in cortisol level in both FHIn the pathophysiology of bipolar disorders (BD), several lines of evidence support the hypothesis of an underlying dysfunction of the serotonergic system. Increased platelet serotonin (5-hydroxytryptamine or 5-HT), a lower maximal velocity (Vmax) of 5-HT platelet uptake and decreased central serotonergic neurotransmitter activity, indicated by decreased 5HIAA/5-HT ratios, have been reported in untreated bipolar depressed patients (Wirz Justice and Puhringer 1978; Marazziti et al.1991;Leake et al. 1991;Young et al. 1994). Polymorphism in the 5-HT-transporter, 5-HT receptors and the tryptophan hydroxylase gene have been associated with the pathophysiology of BD (Kunugi et al. 1997;Oruc et al. 1997;Bellivier et al. 1998).Acute tryptophan depletion (ATD) is a direct method to investigate central serotonergic vulnerability (Delgado et al. 1994). In this procedure, a lowering of central 5-HT Vulnerability in Relatives of Bipolar Patients 8355-HT synthesis is accomplished by giving subjects a 50-100 g balanced amino acid-drink (AA-drink), composed of amino acids, including large neutral amino acids (LNAAs: tyrosine, valine, leucine, isoleucine and phenylalanine), and devoid of tryptophan (Trp) (Young 1991). In remitted depressed patients, ATD induced depressive symptoms (Smith et al. 1997;Aberg-Wistedt et al. 1998;Moreno et al. 2000). In healthy first-degree relatives of depressed patients, ATD induced a modest lowering of mood, compared with healthy control subjects (Benkelfat et al. 1994;Klaassen et al. 1999). It thus appears that individuals without prior depressive episodes, but at a genetic risk for depression, may be biologically predisposed to mood-lowering effects of ATD.Until now, little attention has been paid to the effects of ATD in BD, and results are inconsistent . Cappiello et al. (1997) reported a significant increase in manic symptoms in recently remitted (one month) lithium-treated manic patients. In BD patients who were stable for a longer period (1-15 years), ATD did not induce significant mood changes (Benkelfat et al. 1995;Cassidy et al. 1998;Hughes et al. 2000).In BD patients abnormalities in cortisol homeostas...

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Hypothalamic‐pituitary‐adrenocortical function in mixed and pure mania

Cited by 87 publications

References 26 publications

Assessment of circadian function in fibroblasts of patients with bipolar disorder

Assessment of circadian function in fibroblasts of patients with bipolar disorder

Pattern of Response to Divalproex, Lithium, or Placebo in Four Naturalistic Subtypes of Mania

Effects of Acute Tryptophan Depletion on Mood and Cortisol Release in First-degree Relatives of Type I and Type II Bipolar Patients and Healthy Matched Controls

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