Serotonergic dysfunction in women with pure premenstrual dysphoric disorder: is the fenfluramine challenge test still relevant?

Steiner, Meir; Yatham, Lakshmi N.; Coote, Margaret; Wilkins, Annette; Lepage, Patricia

doi:10.1016/s0165-1781(99)00062-1

Cited by 24 publications

(11 citation statements)

References 32 publications

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“…Fitzgerald et al (1997) showed that women with PMDD had significantly blunted prolactin responses to d,l-fenfluramine during luteal phase in comparison to controls. Steiner et al (1999) found no significant differences in prolactin or cortisol responses to d,l-fenfluramine during luteal or follicular phase between women with and without PMDD. Rasgon et al (2000) showed no significant difference in prolactin or cortisol responses to L-tryptophan across menstrual cycles between women with PMS and controls.…”

Section: Introductioncontrasting

confidence: 54%

“…In any case, at the moment, the concept of PMS may widely cover heterogeneous pathologies, which include women with PMS without PMDD, women with PMDD, and so on. As the previous studies (Bancroft et al 1991;Veeninga and Westenberg 1992;Yatham 1993;Bancroft and Cook 1995;Su et al 1997;Fitzgerald et al 1997;Steiner et al 1999;Rasgon et al 2000) probably dealt with these diseases together, some discrepancy probably occurred among their findings, which might depend on the ratio of PMDD and PMS without PMDD included.…”

Section: Discussionmentioning

confidence: 90%

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Fluctuating serotonergic function in premenstrual dysphoric disorder and premenstrual syndrome: findings from neuroendocrine challenge tests

et al. 2006

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Section: Introductioncontrasting

confidence: 54%

Section: Discussionmentioning

confidence: 90%

Fluctuating serotonergic function in premenstrual dysphoric disorder and premenstrual syndrome: findings from neuroendocrine challenge tests

et al. 2006

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“…First, as reviewed above, allopregnanolone negatively modulates the HPA axis in animal models, and although null findings have been reported (Su et al, 1997;Bloch et al, 2000;Lombardi et al, 2004) where diagnosis-related differences exist, they suggest blunted HPA axis function in PMDD. For example, a number of studies have reported lower circulating ACTH or cortisol concentrations in PMDD women (Rabin et al, 1990;Redei & Freeman, 1993;Girdler et al, 1998), increased ACTH response to ovine CRF (consistent with lower endogenous CRF; Rabin et al, 1990), a delayed (Steiner et al, 1999) or blunted HPA axis response to serotonergic agents (Bancroft et al, 1991;Su et al, 1997), and the absence of the normal plasma cortisol and ACTH response to exercise stress in the luteal phase that is seen in non-PMDD women (Roca et al, 2003). More compelling evidence that the greater allopregnanolone concentrations that we observed in PMDD women might negatively modulate HPA axis function in that population comes from our own results reported in Girdler et al (2001), documenting significantly lower plasma cortisol concentrations in the PMDD women than the controls (5.8±0.6 vs. 7.7±0.7 μg/dL, respectively; P<0.05).…”

Section: Hpa Axis and Gaba A Receptor Function In Pmddmentioning

confidence: 99%

Neurosteroids in the context of stress: Implications for depressive disorders

Girdler

Klatzkin

2007

Pharmacology & Therapeutics

129

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Animal models indicate that the neuroactive steroids 3α,5α-THP (allopregnanolone) and 3α,5α-THDOC (allotetrahydroDOC) are stress responsive, serving as homeostatic mechanisms in restoring normal GABAergic and hypothalamic-pituitary-adrenal (HPA) function following stress. While neurosteroid increases to stress are adaptive in the short term, animal models of chronic stress and depression find lower brain and plasma neurosteroid concentrations and alterations in neurosteroid responses to acute stressors. It has been suggested that disruption in this homeostatic mechanism may play a pathogenic role in some psychiatric disorders related to stress. In humans, neurosteroid depletion is consistently documented in patients with current depression and may reflect their greater chronic stress. Women with the depressive disorder, premenstrual dysphoric disorder (PMDD), have greater daily stress and a greater rate of traumatic stress. While results on baseline concentrations of neuroactive steroids in PMDD are mixed, PMDD women have diminished functional sensitivity of GABA A receptors and our laboratory has found blunted allopregnanolone responses to mental stress relative to non-PMDD controls. Similarly, euthymic women with histories of clinical depression, which may represent a large proportion of PMDD women, show more severe dysphoric mood symptoms and blunted allopregnanolone responses to stress versus never-depressed women. It is suggested that failure to mount an appropriate allopregnanolone response to stress may reflect the price of repeated biological adaptations to the increased life stress that is well documented in depressive disorders and altered allopregnanolone stress responsivity may also contribute to the dysregulation seen in HPA axis function in depression.

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“…Additionally, women often experience mood changes after surgical removal of the ovaries, an effect that can be reversed by hormone replacement therapy [4, 5, 6]. These disorders are also associated with changes in serotonergic function [3, 7, 8]. The underlying cause of these mood disorders may involve changes in serotonergic function due to changes in ovarian hormone levels.…”

Section: Introductionmentioning

confidence: 99%

Ovariectomy-Induced Increases in Hypothalamic Serotonin-1A Receptor Function in Rats Are Prevented by Estradiol

Raap¹,

DonCarlos

García³

et al. 2002

Neuroendocrinology

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The present study investigated the effects of long-term estradiol withdrawal (ovariectomy) on hypothalamic serotonin-1A (5-HT_1A) receptor signaling. Changes in neuroendocrine responses to the 5-HT_1A agonist 8-OH-DPAT and levels of G_z protein in the hypothalamus were used to examine 5-HT_1A receptor signaling. Five days following ovariectomy, rats received daily injections of either 2 µg of β-estradiol 3-benzoate or vehicle (subcutaneously) for 2, 4 or 14 days. Twenty-four hours after the last injection, and 15 min prior to sacrifice, rats were injected with (±)8-OH-DPAT (50 µg/kg, s.c.) or saline. Estradiol treatment did not alter basal corticotropin (ACTH) or oxytocin levels. Injection of (±)8-OH-DPAT produced significant increases in plasma ACTH and oxytocin levels. In the vehicle-treated rats, hormone responses to 8-OH-DPAT were enhanced in rats that received injections for 14 days compared with rats that received injections for either 2 or 4 days. Estradiol treatment for 4 or 14 days blunted this enhanced ACTH response to 8-OH-DPAT, whereas the oxytocin response to 8-OH-DPAT was only blunted after 14 daily injections of β-estradiol 3-benzoate. The treatment with β-estradiol 3-benzoate (2 µg/rat) did not reduce membrane-associated G_z protein levels in the paraventricular nucleus of the hypothalamus. Hence, the inhibitory influence of a low dose of β-estradiol 3-benzoate on 5-HT_1A receptor signaling in the hypothalamus is not accompanied by a change in the levels of G_z protein in the paraventricular hypothalamic nucleus. Results from the present study indicate a supersensitivity of 5-HT_1A receptors after withdrawal of estradiol and suggest that estradiol suppresses 5-HT_1A receptor signaling.

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Serotonergic dysfunction in women with pure premenstrual dysphoric disorder: is the fenfluramine challenge test still relevant?

Cited by 24 publications

References 32 publications

Fluctuating serotonergic function in premenstrual dysphoric disorder and premenstrual syndrome: findings from neuroendocrine challenge tests

Fluctuating serotonergic function in premenstrual dysphoric disorder and premenstrual syndrome: findings from neuroendocrine challenge tests

Neurosteroids in the context of stress: Implications for depressive disorders

Ovariectomy-Induced Increases in Hypothalamic Serotonin-1A Receptor Function in Rats Are Prevented by Estradiol

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