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)

We evaluated the effects on bone mineral density (BMD) of a 12-month treatment with goserelin depot, a gonadotropin-releasing hormone agonist, in a group of women with symptomatic uterine myomas requiring hysterectomy. Sixteen women, mean age 45.6 +/- 5.0, reporting menorrhagia associated with uterine myomas, candidates for hysterectomy, were scheduled to be treated with goserelin depot for 12 months. BMD was measured at the vertebral (L2-L4) and proximal femur level (femoral neck and trochanter) at the start of therapy and 6, 12, and 18 months later using dual energy X-ray absorptiometry (Hologic QDR 1000/W). The patients were followed for a minimum of 6 months after the end of treatment. Thirteen of the 16 women enrolled completed the treatment and three suspended it after 5, 6, and 7 months, respectively, because of side effects (hot flashes, insomnia, depression). Of the 13 women who completed the treatment, three underwent hysterectomy because of myoma regrowth and the recurrence of symptoms 3-18 months later; four reached the menopause 5-16 months later, and six were all menstruating normally with a follow-up varying from 6 to 18 months. After 12 months of therapy we observed a bone loss at vertebral, femoral neck, and trochanter of 4.4% (P < 0.05 versus baseline; P = not significant versus 6 months), 7.5% (P < 0.01 versus baseline, P < 0.01 versus 6 months), and 7.6% (P < 0.001 versus baseline, P < 0.05 versus 6 months), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects on bone mineral density of 12-month goserelin treatment in over 40-year-old women with uterine myomas. 767 Nov 71

In distinction to the course of reproductive ageing in women, men do not experience a rapid decline of Leydig cell function or irreversible arrest of reproductive capacity in old age. Hence, strictu sensu, the andropause does not exist. Nevertheless, both spermatogenesis and fertility as well as Leydig cell function do decline with age, as shown by a decrease of +/- 35% of total and of 50% of free testosterone levels between the age of 20 and 80 years. The origin of this decline of Leydig cell function resides on the one hand in the testes, and is essentially characterized by a decreased number of Leydig (and Sertoli) cells and on the other hand in the hypothalamo-pituitary complex characterized by a decreased luteinzing hormone (LH) pulse amplitude, LH pulse frequency being maintained. As the responsiveness of the gonadotrophs to gonadotropin-releasing hormone (GnRH) remains unimpaired, one may assume that the amount of GnRH released at each pulse is also reduced, possibly as the consequence of a reduction of the cellular mass of GnRH neurones. Plasma levels of testosterone below the lower normal limit occur, however, only in a minority of elderly men from 7% in the age group 40-60, to 20% in the age group 60-80 and 35% in the age group over 80 years old. Factors influencing testosterone levels in elderly men are multiple: hereditary, environmental (obesity, stress), psychosocial (depression, smoking, drugs) or socioeconomical (diet, hygiene). Whether these elderly men should be substituted with androgens remains controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ageing of the hypothalamo-pituitary-testicular axis in men. 772 Dec 58

Although hormonal response abnormalities in depression have been demonstrated in several hypothalamic-pituitary-target organ axes after a variety of neuroendocrine challenge tests, studies of hypothalamic-pituitary-gonadal (HPG) axis function have been inconsistent in their findings. The use of maximal or supramaximal doses of gonadotropin-releasing hormone (GnRH) in early studies (150-600 micrograms) may have masked the presence of more subtle disturbances in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responsiveness in depression. We hypothesized that submaximal doses of GnRH might reveal a more subtle dysregulation in gonadotropin responsiveness in depression, and therefore measured LH and FSH responses after GnRH 10 micrograms and 90 micrograms doses in nine premenopausal depressed women and six healthy controls. There were no statistically significant differences between subject groups for mean basal LH, FSH, and estradiol concentrations, nor for any of the LH and FSH response values after either GnRH stimulation dose. The present observations of an intact HPG axis in depression contrast with findings of disturbances in most other hypothalamic-pituitary axes, and suggest that neuroendocrine dysregulation in depression might not represent a generalized limbic system-hypothalamic-pituitary abnormality, but rather a more restricted lesion sparing the medial preoptic and/or arcuate region of the hypothalamus which regulates gonadotropin secretion.
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PMID:Gonadotropin (LH and FSH) response after submaximal GnRH stimulation in depressed premenopausal women and healthy controls. 777 59

1. The sympathetic superior cervical ganglia (SCG) provide innervation to the pineal gland and median eminence through the internal carotid nerve and to the thyroid and parathyroid glands through the external carotid nerve. 2. Postsynaptic activation in median eminence nerve endings shortly after superior cervical ganglionectomy (SCGx) was accompanied by a depression of LH and FSH release and by a 3-5 day delay in rat estrous cyclicity. A decrease in TSH and GH release and an increase in ACTH and prolactin release were also found. These effects were accompanied by a) an increase in medial basal hypothalamic (MBH) LHRH, TRH and GHRH, b) a decrease in MBH somatostatin, AVP and CRH, and c) a normal adenohypophyseal response to hypophysiotropic hormones. Neurohypophyseal AVP release decreased during degeneration of sympathetic nerve terminals in the neurohypophyseal lobe after SCGx. The effects were generally mediated by alpha 1-adrenoceptors and were pineal gland. 3. In thyroid and parathyroid tissue the following events were observed during the wallerian degeneration phase after SCGx: a) alpha 1-adrenoceptor inhibition of thyroxine (T4) release, b) alpha 1-adrenoceptor inhibition, together with beta-adrenoceptor stimulation, of calcitonin release, and c) alpha 1-adrenoceptor inhibition of parathyroid hormone release. Thyroid sympathetic nerves also modulate slow phenomena such as compensatory thyroid growth after partial thyroidectomy. 4. In rats subjected to cholinergic decentralization of the thyroid gland, a decrease of plasma T4 and an increase of plasma TSH, as well as an impaired goitrogenic and thyroid compensatory response were detectable. The calcitonin and PTH response to changes in calcium levels increased after regional parasympathetic denervation. 5. The results indicate that cervical autonomic nerves constitute a parallel pathway through which the brain communicates with the endocrine system.
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PMID:Peripheral neuroendocrinology of the cervical autonomic nervous system. 808 Dec 83

In the menopause transition, ovarian steroid production is gradually inhibited and around 35% of women will seek medical help for postmenopausal symptoms. The hot flush is a characteristic manifestation occurring in about 70% of women; it is associated with oestrogen withdrawal and disappears with oestrogen-based hormone replacement therapy. The exact mechanism behind it is still unclear but is probably related to heat loss mechanisms. The flush often occurs in parallel to changes in skin temperature, blood flow, pulse rate and pulses of luteinizing hormone (LH). These are probably secondary to a disturbance in the thermoregulatory centre of the CNS, which is anatomically close to neurons containing gonadotropin-releasing hormone. Depression is no more frequent in the menopausal transition than at other times in life. After surgical menopause, however, oestrogen improves low mood over placebo. In women with premenstrual syndrome, an increased feeling of well-being is associated with the pre-ovulatory oestrogen peak. Progestogens are associated with negative mood changes during the menstrual cycle, oral contraception and postmenopausal replacement therapy. Certain progesterone metabolites are anaesthetic and have anti-epileptic and anxiolytic properties, effects which are mediated via the type A gamma-aminobutyric acid (GABAA) receptor. Oestrogen is associated with increased sensory perception, locomotory activity, limb coordination and balance: this may help explain the increased frequency of bone fractures in the early postmenopausal period. Oestrogen improves memory and performance in patients with mild Alzheimer's dementia and increases epileptic activity in patients with partial epilepsy. These effects can be related to amplifying effects of oestrogen on excitatory amino acids in the CNS.
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PMID:Symptoms related to the menopause and sex steroid treatments. 858 96

To determine the extent of dysregulation of gonadotropin secretion in depressed women, we measured nocturnal and diurnal serum luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations and the responses of these hormones to gonadotropin releasing hormone (LHRH) in 20 Research Diagnostic Criteria primary, definite endogenous female depressives and in 20 individually matched female normal controls. Fourteen patients and 14 controls were premenopausal, and six patients and six controls were peri/postmenopausal or panhysterectomized. None of the latter was receiving estrogen replacement therapy. The premenopausal patients showed no significant differences in basal nocturnal or diurnal gonadotropin concentrations and no significant differences in hormone concentrations post-LHRH compared to their premenopausal matched controls. In contrast, in the postmenopausal subjects there were (1) significantly increased diurnal vs. nocturnal serum FSH concentrations in the depressives; (2) marginally increased nocturnal, diurnal, and LHRH-stimulated LH concentrations and highly significantly increased LHRH-stimulated FSH concentrations in the depressives compared to their controls; and (3) positive correlations between the LH measures and ratings of depression severity in the patients. These results suggest a dysregulation of the HPG axis in peri/postmenopausal and panhysterectomized female endogenous depressives.
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PMID:Neuroendocrine aspects of primary endogenous depression--XIV. Gonadotropin secretion in female patients and their matched controls. 858 1

The effect of pretreatment with the gonadotropin releasing hormone (GnRH) agonist D-Trp6-LHRH (Decapeptyl) on platelet serotonin transporter in women undergoing assisted reproductive treatment (ART) was investigated and compared with women treated with human menopausal gonadotropin (Pergonal). The study group (n = 10) was exposed for 12 days to 3.2 mg Decapeptyl C.R. while a comparison group (n = 9) was exposed to 11 days of human meno-pausal gonadotropin (Pergonal). All patients were assessed with the Hamilton depression and anxiety scales before and after treatment, and platelet and plasma samples were collected at the same time points. Plasma levels of estradiol, progesterone. FSH and LH were determined by radioimmunoassay (RIA). Platelet serotonin transporter was labeled using high affinity [3H]imipramine binding. The GnRH analogue induced ovarian suppression as reflected by low plasma estradiol levels, while Pergonal administration induced ovarian stimulation. An elevation in the Hamilton depression and anxiety scale scores was observed in the Decapeptyl treated group; this mood alteration was associated with a significant decrease (19%, P < 0.05) in the density (Bmax) of platelet [3H]imipramine binding sites. No significant change was observed in the Bmax of the Pergonal treated group. These results indicate that ovarian suppression (menopausal-like state) in young women is associated with depressed and anxious mood and decreased serotonin transporter density.
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PMID:Chronic GnRH agonist administration down-regulates platelet serotonin transporter in women undergoing assisted reproductive treatment. 878 88

The neuropeptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) play a key role in sleep endocrine regulation. After pulsatile application of GHRH during the first few hours of the night in young normal controls SWS and GH increase, whereas cortisol is blunted. CRH however prompts inverse effects. The balance between these peptides is changed in favour of CRH physiologically during the second time of the night, during the acute episode of depression (due to overactivity of GRH) and in the elderly (due to reduced activity of CHRH). These changes explain the aberrances of sleep endocrine activity in these states, as shallow sleep, low GH and enhanced cortisol.
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PMID:[The role of neuropeptides in normal and disordered sleep regulation]. 901 57

The hypothalamic-pituitary-adrenal axis exerts profound, multilevel inhibitory effects on the female reproductive system. Corticotropin-releasing hormone (CRH) and CRH-induced proopiomelanocortin peptides inhibit hypothalamic gonadotropin-releasing hormone secretion, whereas glucocorticoids suppress pituitary luteinizing hormone and ovarian estrogen and progesterone secretion and render target tissues resistant to estradiol. The hypothalamic-pituitary-adrenal axis is thus responsible for the "hypothalamic" amenorrhea of stress, which is also seen in melancholic depression, malnutrition, eating disorders, chronic active alcoholism, chronic excessive exercise, and the hypogonadism of the Cushing syndrome. Conversely, estrogen directly stimulates the CRH gene promoter and the central noradrenergic system, which may explain adult women's slight hypercortisolism; preponderance of affective, anxiety, and eating disorders; and mood cycles and vulnerability to autoimmune and inflammatory disease, both of which follow estradiol fluctuations. Several components of the hypothalamic-pituitary-adrenal axis and their receptors are present in reproductive tissues as autacoid regulators. These include ovarian and endometrial CRH, which may participate in the inflammatory processes of the ovary (ovulation and luteolysis) and endometrium (blastocyst implantation and menstruation), and placental CRH, which may participate in the physiology of pregnancy and the timing of labor and delivery. The hypercortisolism of the latter half of pregnancy can be explained by high levels of placental CRH in plasma. This hypercortisolism causes a transient postpartum adrenal suppression that, together with estrogen withdrawal, may partly explain the depression and autoimmune phenomena of the postpartum period.
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PMID:Interactions between the hypothalamic-pituitary-adrenal axis and the female reproductive system: clinical implications. 969 32

The inhibitory control of growth hormone (GH) release by somatostatin (SRIH) has been conserved throughout vertebrate evolution. In contrast, the neuropeptides involved in the stimulatory control of GH vary according to species and/or physiological situations. We investigated the direct pituitary regulation of GH release in a primitive teleost, the European eel (Anguilla anguilla L.) at the juvenile stage. Short-term serum-free primary cultures of dispersed pituitary cells were used, and GH release was measured by an homologous radioimmunoassay. Whereas growth hormone-releasing hormone (GHRH), gonadotropin-releasing hormone (GnRH), thyrotropin-releasing hormone (TRH), neuropeptide Y (NPY) and cholecystokinin (CCK) failed to induce any change in GH release, corticotropin-releasing hormone (CRH) dose-dependently stimulated GH release with a significant effect at 1 nM and a maximal effect (> or =400% of controls at 24 h) at 100 nM. In agreement with our previous studies, PACAP also stimulated GH release but its maximal effect was lower than that of CRH. Proopiomelanocortin (POMC)-peptides, corticotropin (ACTH), melanotropin (alpha-MSH), beta-endorphin) had no effect on GH release, at any dose tested (0.1-1000 nM), indicating that the stimulatory effect of CRH on GH release by somatotrophs was not mediated by CRH-induced release of POMC-peptides from corticotrophs and melanotrophs. The CRH antagonist, alpha-helical CRH(9-41), significantly inhibited the stimulatory effect of CRH on GH release, suggesting the implication of specific CRH receptors related to mammalian ones. The stimulatory effect of CRH on GH release was reduced after 24 h of incubation, indicating a desensitization. In contrast, no desensitization to the inhibitory effect of SRIH was observed. SRIH inhibited CRH action in a dose-dependent manner. The effect of SRIH was overriding, 1 nM SRIH being able to abolish the effect of 1000 nM CRH. In conclusion, in the eel, CRH stimulates GH release directly at the pituitary cell level. GH and cortisol secretions could interact in controlling several physiological functions such as metabolism and ion exchange. This study suggests that CRH may have played an important early role in vertebrates co-ordinating the activation of various endocrine axes involved in metamorphosis, osmoregulation, stress and fasting. The stimulatory role of CRH on GH release may have been partially conserved during evolution, as it is found in some human physio-pathological situations such as stress, fasting and depression.
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PMID:Evidence that corticotropin-releasing hormone acts as a growth hormone-releasing factor in a primitive teleost, the European eel (Anguilla anguilla). 1032 May 66


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