Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and laboratory studies suggest that progesterone reduces epileptic seizure activity. The mechanisms underlying this effect are not known. The present study determined the effects of progesterone on extracellular evoked responses recorded in the CA1 field of hippocampal slices, as well as epileptiform responses recorded from tetanized slices. Slices were prepared from ovariectomized rats, with or without estrogen replacement. Hippocampal slices were superfused in vitro with one of the following treatments: progesterone with or without RU486 (a progesterone receptor antagonist); allopregnanolone (a progesterone metabolite that potentiates GABA action at GABA(A) receptors); RU5020 (a high-affinity progesterone receptor agonist); or cholesterol (control). In non-tetanized slices, a twofold increase in the excitatory postsynaptic field potential and population spike amplitude occurred during both cholesterol and progesterone superfusion. In contrast, under the same conditions, exposure to allopreganolone caused a 25% reduction in both field potential and population spike amplitude of evoked responses within 30min of treatment. In tetanized slices, progesterone and RU5020, but not allopregnanolone or cholesterol, caused significant reductions in the field potential and population spike amplitude of evoked responses. Progesterone and RU5020 also significantly reduced the duration of tetanic stimulus-induced afterdischarges and the frequency of spontaneous interictal discharges. The effects of allopregnanolone were restricted to a reduction in the primary afterdischarge duration. Estrogen replacement slightly attenuated progesterone's suppression of spontaneous discharges and depression of evoked responses. All responses to progesterone were blocked by prior or concurrent exposure to RU486. These data indicate that allopregnanolone suppresses evoked potentials in non-tetanized hippocampal slices, consistent with previous reports that this neurosteroid has marked anxiolytic and anticonvulsant effects. After tetanization, however, progesterone receptor-mediated responses become quantitatively more important as a mechanism for suppressing hippocampal electrical activity.
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PMID:Progestin receptors mediate progesterone suppression of epileptiform activity in tetanized hippocampal slices in vitro. 1111 38

Estrogen exerts profound effects on mood and mental state. The ability of estrogen to modulate serotonergic function raises the possibility that it may play a role in the mechanism associated with depression and its treatment. A cellular mechanism for estrogen to influence mood might be through the regulation of genes involved at various levels of the serotonin system. Here we report that estrogen can up-regulate the expression of the serotonin-1A receptor via a new mechanism involving synergistic activation by nuclear factor-kappa B (NF-kappa B) with estrogen receptor alpha. Interestingly, we observed that only estrogen receptor-alpha, and not -beta, was able to mediate this effect of estrogens. The partial antiestrogen, 4-hydroxytamoxifen, had the same effect as estrogen. In addition, mutation analysis showed that both the transactivation function of p65 and activation function 1 of estrogen receptor-alpha were essential for this synergistic regulation. Therefore, we propose that NF-kappa B complexes cooperate with estrogen receptor-alpha to recruit cofactors into the complex and thereby synergistically activate the serotonin-1A receptor promoter through nonclassical estrogen response elements by a mechanism that does not involve direct receptor binding to DNA.
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PMID:Synergistic activation of the serotonin-1A receptor by nuclear factor-kappa B and estrogen. 1126 6

How a weakened immune system affects the female's reproductive system is explained. The female's endocrine system controls the menstrual and reproductive systems, and the immune system attacks harmful substances and organisms. The hypothalamus stimulates the pituitary gland to produce the hormones FSH and LH, which in turn signal the ovaries to produce estrogen and progesterone. These hormones cause a mature egg to be released. If fertilized, the egg remains within the uterus; if not, menstruation occurs. HIV-positive females often complain of menstrual cycle changes, such as irregular periods, depression, or pain. The virus, other complications, or medications, such as AZT, may cause these symptoms. Estrogen therapy may help those with suppressed immune systems who have premature menopause. Oral contraceptives offer protection against pregnancy, but not HIV. It is not known if the pill reacts adversely with AIDS treatment drugs. Lists are provided showing the pros and cons of oral contraceptives and hormone therapy.
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PMID:[Women, immunity and sexual hormones]. 1136 3

Changes in the perinatal testosterone surge have been related to demasculinization of the central nervous system and androgen-dependent growth of the reproductive organs in male mammals. Earlier reports suggest that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interferes with androgen production, but the perinatal effects have remained elusive. In the present study we explored in utero-effects of TCDD (0.05, 0.1, 0.5, and 1.0 microg/kg), introduced on day 13.5 of pregnancy, on prenatal (day 19.5 post-conception [p.c.]) testosterone (T) surge and pituitary luteinizing hormone (LH) production in TCDD-resistant Han/Wistar (H/W) and TCDD-sensitive Long-Evans (L-E) rats. To elucidate estrogenic effects on T and LH production, Sprague-Dawley (S-D) fetuses with previously known DES-sensitivity were exposed in utero to diethylstilbestrol (DES, 100-300 microg/kg) on days 13.5, 15.5, and 17.5 p.c. For comparison, H/W fetuses that responded to TCDD treatments were exposed to DES at concentration of 100 microg/kg. It was found that TCDD has a stimulatory effect on testicular T synthesis in the H/W fetuses and that their circulating T concentrations increased significantly. The effect was not seen in the inbred L-E fetuses, which throughout the study showed considerably low testicular T levels. Pituitary LH concentrations also increased in the H/W fetuses exposed to TCDD. Effects of TCDD (1.0 microg/kg) in the H/W fetuses could be confirmed in vitro by human chorionic gonadotropin (hCG) stimulation assay showing the highest response rate in the TCDD exposed testes. Stimulation of cyclic AMP (adenosine-3', 5'-cyclic monophosphate[cAMP]) production was not considerably altered by in utero TCDD exposure. A significant depression in testicular and plasma T content was seen in the DES-exposed S-D and H/W fetuses, but pituitary LH levels did not alter considerably. In the presence of hCG, DES-exposed testes showed lower in vitro T and cAMP production rates compared to the untreated testes. TCDD (1.0 microg/kg) increased and DES decreased the male body weight gain, but the changes were not sex-dependent. It is concluded that TCDD may increase the amplitude of the prenatal testosterone surge in male rats by stimulating pituitary LH production and enhancing the sensitivity of the fetal testis to LH. DES, on the contrary, apparently impairs testicular steroidogenesis and pituitary function.
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PMID:Prenatal testosterone and luteinizing hormone levels in male rats exposed during pregnancy to 2,3,7,8-tetrachlorodibenzo-p-dioxin and diethylstilbestrol. 1140 7

The benefit of treating postmenopausal women with established cardiovascular disease with combined estrogen-progestogen hormone replacement therapy (HRT) is controversial. This study investigated the effect of treatment with estradiol and norethisterone acetate on exercise tolerance and on the frequency and severity of ischemic attacks in postmenopausal women with stable angina pectoris. A total of 74 Chinese women were recruited for this 16-week double-blind, placebo-controlled trial. They were randomly allocated into two groups; one group received placebo/placebo/placebo and the other group received placebo/estrogen-progestogen/placebo. Estrogen-progestogen continuous combined HRT increased both time to 1-mm ST depression (99.1 s, p < 0.05) compared with a mean decrease of 22.9 s with placebo (p < 0.05), and total exercise duration also showed a significant increase (32.7 s, p < 0.05) after treatment compared with placebo (2.5 s, p < 0.05). In addition, the total number of ischemic events/24 h during ambulatory electrocardiographic monitoring decreased by 0.82 events after treatment (p < 0.05) compared with an increase in the placebo group (0.94), a highly significant difference (p = 0.006). These results suggest that the administration of this particular combined hormone replacement preparation may have a beneficial effect on myocardial ischemia in postmenopausal women with established coronary disease.
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PMID:Anti-ischemic action of estrogen-progestogen continuous combined hormone replacement therapy in postmenopausal women with established angina pectoris: a randomized, placebo-controlled, double-blind, parallel-group trial. 1148 42

Treatment of major depression in menopausal women is controversial. Estrogen replacement therapy (ERT) treats mild depression but may not treat more severe depression in this population. Antidepressants are recommended as treatment for major depression in menopausal women, but the specific efficacy of antidepressants has not been examined in menopause-associated depression. Twenty-two perimenopausal and postmenopausal women aged 40-61 taking stable doses of ERT who met Structured Clinical Interview for DSM-IV (SCID-IV) criteria for major depression were accessioned into an open-label clinical trial of mirtazapine. Subjects were treated with 30-45 mg/day mirtazapine for 8 weeks and were assessed every 2 weeks with the Hamilton Depression Rating Scale-17 (HDRS-17), Beck Depression Inventory (BDI), and Clinical Global Impression (CGI) Scale. Remission of depression was defined as an HDRS-17 score < or =7 at the week 8 study visit. Sixteen (73%) of the enrolled subjects completed the 8-week study. The median HDRS-17 score declined from 20.5 (range 12-37) at baseline to 2 (range 0-9) at week 8 (Wilcoxon signed-rank test, p < 0.001). Remission of depression was achieved by 14 of 16 (87.5%) study completers. Subjects responded well to mirtazapine regardless of whether their depression preceded ERT use or developed after ERT was initiated. Therapeutic response also appeared independent of menopausal status (perimenopausal vs. postmenopausal), ERT preparation, and concomitant use of medroxyprogesterone. Mirtazapine is an effective treatment for major depression in perimenopausal and postmenopausal women whose depression precedes ERT use and does not respond to ERT or whose depression develops after ERT is initiated.
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PMID:An open trial of mirtazapine in menopausal women with depression unresponsive to estrogen replacement therapy. 1178 10

Although dissociative phenomena are often transient features of mental states, existing measures of dissociation are designed to measure enduring traits. A new present-state self-report measure, sensitive to changes in dissociative states, was therefore developed and psychometrically validated. Fifty-six items were formulated to measure state features, and sorted according to seven subscales: derealization, depersonalization, identity confusion, identity alteration, conversion, amnesia and hypermnesia. The State Scale of Dissociation (SSD) was administered with other psychiatric scales (DES, BDI, BAI, SCI-PANSS) to 130 participants with DSM-IV major depressive disorder schizophrenia, alcohol withdrawal, dissociative disorders and controls. In these sample populations, the SSD was demonstrated as a valid and reliable measure of changes in and the severity of dissociative states. Discriminant validity, content, concurrent, predictive, internal criterion-related, internal construct and convergent validities, and internal consistency and split-half reliability were confirmed statistically. Clinical observations of dissociative states, and their comorbidity with symptoms of depression and psychotic illness, were confirmed empirically. The SSD, an acceptable, valid and reliable scale measuring state features of dissociation at the time of completion, was obtained. This is a prerequisite for further investigation of correlations between changes in dissociative states and concurrent physiological parameters.
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PMID:Psychometric validation of the State Scale of Dissociation (SSD). 1200 98

Osteopenia, which is correlated with amenorrhea and poor nutritional habits, has been well documented in elite ballet dancers. Estrogen replacement therapy and recovery from amenorrhea have not been associated with normalization of bone density. Thus, the osteopenia may be related to changes brought about by chronic dieting or other factors, such as a hypometabolic state induced by poor nutrition. The purpose of this study was to investigate the relationship of chronic dieting and resting metabolic rate (RMR) to amenorrhea and bone density. RMR, bone density, eating disorder assessments, leptin levels, and complete menstrual and medical histories were determined in 21 elite ballet dancers and in 27 nondancers (age, 20-30 yr). No significant correlations were found between high EAT26 scores, a measure of disordered eating, and RMR, bone densities, body weight, body fat, or fat-free mass. However, when RMR was adjusted for fat-free mass (FFM), a significant positive correlation was found between RMR/FFM and bone density in both the arms (P < 0.001) and spine (P < 0.05) in ballet dancers, but not in the normal controls. The dancers also demonstrated significantly higher EAT scores (22.9 +/- 10.3 vs. 4.1 +/- 2.4; P < 0.001) and lower RMR/FFM ratios (30.0 +/- 2.2 vs. 32.05 +/- 2.8; P < 0.01). The only variable to predict lower RMR/FFM in the entire sample was ever having had amenorrhea; this group had significantly higher EAT scores (18.0 +/- 13.5 vs. 10.3 +/- 10.2; P < 0.05), lower leptin levels (4.03 +/- 0.625 vs. 7.10 +/- 4.052; P < 0.05), and lower bone mineral density in the spine (0.984 +/- 0.11 vs. 1.10 +/- 0.13; P < 0.05) and arm (0.773 +/- 0.99 vs. 0.818 +/- 0.01; P < 0.05). We hypothesize that the correlation between low RMR and lower leptin levels and bone density may be more strongly related to nutritional habits in ballet dancers, causing significant depression of RMR, particularly for those with a history of amenorrhea.
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PMID:Bone density and amenorrhea in ballet dancers are related to a decreased resting metabolic rate and lower leptin levels. 1205 Feb 50

It is estimated that 17% of our population will be over the age of 65 by the year 2030. As the body ages, many physiologic processes begin to decline. Health-care providers will need to be well-educated in the many sequelae of aging. Practitioners will especially need to focus on the health-care needs of women, since women have a longer life expectancy than men. Estrogen deprivation occurs in all women. Some will not have any symptoms, while others may experience all of its debilitating side effects: hot flashes, osteoporosis, insomnia, irritability, depression, and urogenital atrophy. Even though the latter is not life-threatening, it can alter a woman's quality of life considerably. Because it is easily treatable with minimal risk, all practitioners should become familiar with its presentation and management. This article discusses the many sequelae of urogenital atrophy: vulvovaginal irritation, urinary tract irritative symptoms and infection, urinary incontinence, and sexual dysfunction. Diagnosis and current management strategies are also discussed in detail.
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PMID:Urogenital atrophy: diagnosis, sequelae, and management. 1215 Jul 59

The role of estrogen in the treatment of depression is reviewed. The relation is examined in studies of perimenopausal and postmenopausal women with depressed mood, in studies of depressive disorders, and in studies of estrogen as an adjunct to antidepressant medication. The literature has many methodologic shortcomings, including combining women of various ages, failure to confirm life stage, the use of different types of estrogens, the inclusion of women with a range of mood disturbances, and the enrollment of women with concurrent psychiatric illness. There are few controlled evaluations of the use of estrogen to supplement ongoing antidepressant treatment. Estrogen alone seems to be beneficial for improving mood in perimenopausal and postmenopausal women. Estrogen is superior to placebo for reproductive-related mood disorders, including postpartum depression and mild depressive disorders during perimenopause. Replication is necessary, especially in moderate to severe levels of major depression. Estrogen may augment antidepressant treatment. Assessment and treatment implications are discussed.
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PMID:Role of estrogen in the treatment of depression. 1242 8


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