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)

Acute toxicity studies of [Ac-D-NAL(2)1,4FD-Phe2,D-Trp3,D-Arg6]-LHRH (LHRH-A), a potent antagonist of LHRH were performed. Subcutaneous administration of this peptide to rats induced transient edema of the face and extremities. This effect was maximal 3-5 h after peptide administration and subsided by 24 h. These effects were not seen with an LHRH agonist or two other antagonists. This side effects of LHRH-A was peculiar to rats and not observed in mice, rabbits and rhesus monkeys. Intravenous administration led within minutes to depression of spontaneous activity in rats and monkeys. We conclude that some LHRH antagonists produce species specific effects on vascular permeability and spontaneous activity.
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PMID:[Ac-D-NAL(2)1,4FD-Phe2,D-Trp3,D-Arg6]-LHRH, a potent antagonist of LHRH, produces transient edema and behavioral changes in rats. 637 59

Arginine vasotocin was injected into the third ventricle or intravenously in conscious, ovariectomized rats and its effect on gonadotropin and prolactin release evaluated. The peptide lowered plasma levels of both LH and prolactin in doses of 40 or 100 ng given intraventricularly. The higher dose was slightly more effective than the lower dose. Intravenous injection of a 1-microgram dose of vasotocin failed to alter plasma LH in the ovariectomized animals; however, a 5-micrograms dose induced a slight depression apparent at only 60 min following injection. Intravenous injection of 1 microgram produced a significant lowering of plasma prolactin, whereas a dramatic lowering followed the injection of the higher dose. Plasma FSH was unaffected in these experiments. Incubation of dispersed anterior pituitary cells from ovariectomized rats with various doses of vasotocin revealed no effect of the peptide on the release of FSH, LH, or prolactin. It also did not alter the response to LHRH, but it partially blocked the action of dopamine to inhibit prolactin release. The data indicate that quite low doses of arginine vasotocin act within the brain to inhibit LH and prolactin secretion in ovariectomized, conscious animals.
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PMID:Effects of arginine vasotocin on levels of plasma gonadotropins and prolactin in ovariectomized conscious rats. 640 23

Morphologic changes in the male reproductive system of mongrel dogs immunized against LHRH were quantitated using linear measurements and morphometric techniques at the light-microscopic level. Two experimental groups (5 nonimmunized control animals and 5 actively immunized animals) were killed 12 weeks after the primary immunization. No significant differences were observed between three immunized dogs having low LHRH antibody titers (immunized-unaffected) and the five nonimmunized control dogs. The two immunized dogs (affected) with the highest antibody titers against LHRH were characterized by atrophy and dedifferentiation of the testes, prostate, and excurrent ducts. The morphologic changes in the testes of these two dogs were striking and included an apparent arrest or significant reduction in the spermatogenic process, concurrent epithelial degeneration, and apparent diminution of Leydig cell mass. Drastic reductions in the size of the prostatic acini and epithelial cells, as well as loss of secretory granules, reflected depression of function and androgen production. Similarly, in the excurrent ducts decreases in the measured parameters and loss of regional cytoplasmic specialization denoted functional decrescence. This study demonstrates the regressive effects of LHRH immunoneutralization on the morphology of the reproductive system in the male dog and further supports the feasibility of this system as an animal model for the study of isolated gonadotropin deficiency.
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PMID:Animal model of isolated gonadotropin deficiency. II. Morphologic responses to LHRH immunoneutralization. 641 70

Neuroendocrine strategies in affective disorders have explored both resting values of hormones and hormonal responses to stimuli such as hypoglycemia, TRH, LHRH, dexamethasone, methadone and morphine. The abnormalities established to date have involved growth hormone, cortisol and TSH responses in particular. Prolactin has not been investigated to the same extent. We therefore describe several prolactin studies exemplifying selected neuroendocrine strategies. Our studies of prolactin responses included acute cases of either primary or secondary depression, stabilized bipolar patients, and healthy controls both off and on lithium. We found prolactin response to hypoglycemia significantly reduced in primary but not secondary depressions. Lithium administration led to flattened prolactin responses to hypoglycemia in stabilized bipolar patients but not in healthy controls. The flattened response in patients was observed already after 3 weeks of lithium, and remained flattened after years of treatment. The findings suggest a greater degree of prolactin response reduction in those patients showing most pronounced stability on lithium treatment.
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PMID:Neuroendocrine strategies in affective disorders. 642 Aug 43

Considerable attention has been paid to studies of hormonal response abnormalities in depressed patients, and functional changes have been demonstrated in a number of neuroendocrine axes. The findings from the present study extend the results of previous investigations but demonstrate a functionally intact HPG axis in depressed patients. A number of statements can be made concerning the gonadotropin-releasing hormone (GnRH) strategy: (1) Previous studies utilizing GnRH challenge have been limited in number and poorly controlled. (2) We chose to utilize our normative data because standard gonadotropin response ranges to GnRH have not previously been established in studies with depressed patients. Moreover, hormonal responses may be affected by age, sex, menstrual status, dose, and method and rate of GnRH administration. The assessment of the hormonal responses to GnRH in depressed patients and healthy controls studied under identical conditions provides the most accurate basis for comparison. (3) The incidence of abnormal LH and FSH release in depressed subjects was similar to controls, in contrast to response abnormalities found with other neuroendocrine axes. (4) Alterations in gonadotropin were limited to FSH, were sporadic, and did not differ significantly from controls. This finding is of interest and suggests that neuroendocrine alterations in depression do not necessarily affect all neuroendocrine axes.
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PMID:Gonadotropin release after administration of GnRH in depressed patients and healthy volunteers. 645 52

The blockade in the rat of the estrous FSH surge was investigated by the injection of anti-LHRH serum in order to clarify whether LHRH controls this postovulatory surge as well as the preovulatory LH-FSH surge. A single iv injection of anti-LHRH serum at 1300 h on proestrus not only inhibited ovulation but also eliminated both the preovulatory LH-FSH surge and the second FSH surge in estrus. A single iv injection of anti-LHRH serum at 2200 h on proestrus after the LH-FSH surge did not inhibit either the estrous FSH surge or ovulation, although plasma LH was lowered, and the number of ova ovulated was reduced. Depression of plasma FSH and LH levels was also observed after a single iv injection of pentobarbital sodium (Nembutal; 35 mg/kg BW) at 1300 h on proestrus, but no such effect was observed when pentobarbital was injected at 2200 h on proestrus. A single injection of 10 IU hCG at 1800 h on diestrous II induced precocious ovulation and a concomitant increase in FSH secretion. It was not possible to inhibit the induced secretion of FSH and ovulation by a simultaneous injection of anti-LHRH serum, but plasma LH was completely suppressed. These results demonstrate that the second FSH surge is not controlled by LHRH.
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PMID:Regulation of the second surge of follicle-stimulating hormone; effects of antiluteinizing hormone-releasing hormone serum and pentobarbital. 678 59

Endocrinological investigation of depressed patients shows a wide variety of abnormalities, most of them reflecting disturbed hypothalamo-hypophyseal control mechanisms. Reported results however vary widely among investigators reflecting the heterogeneity of the clinical cases and the difficulties of quantifying depression. The authors report data on 1(0) TSH, PRL and HGH secretion after TRH in a group of 19 endogenous depressed patients; 2(0) insulin secretions after a glucose load in endogenous (10 cases) and neurotic (13 cases) depression; 3(0) LH and FSH secretion after LHRH in 10 neurotic depressed men. The results are compared with those reported in the literature. Their possible contribution to the differential diagnosis of neurotic versus endogenous depression is discussed.
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PMID:[Endocrinological abnormalities in the neurotic states and in depression (author's transl)]. 679 64

LHRH and its analogues produce profound antireproductive effects in both sexes of a variety of animal species. Although the LHRH agonists induce gonadotropin release, gonadal steroid secretion, ovulation, and spermatogenesis as an expression of their traditional profertility pharmacologic profile, they paradoxically and characteristically cause predominant antifertility effects which have been extensively evaluated for potential contraceptive purposes. These agonists produce their antireproductive effects in both males and females by common mechanisms, ultimately resulting in disruption of pituitary-gonadal function, depression of steroidogenesis, and inhibition of target organs dependent on such gonadal support. Similar antireproductive effects have been observed with the LHRH antagonists which competitively inhibit LHRH-induced gonadotropin secretion resulting in reduced blood gonadal steroid levels. Use of the inhibitory properties has been extended to cancer therapy based on the ability of the LHRH analogues (particularly the agonists) to inhibit the growth of steroid-dependent (responsive) tumors (e.g., mammary, prostate) similar to that produced by gonadectomy and antisteroid treatments. The use of these peptides for selected hormone-sensitive tumors presents a novel pharmacotherapeutic application for this class of drug.
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PMID:From contraception to cancer: a review of the therapeutic applications of LHRH analogues as antitumor agents. 681 May 59

A study was undertaken to further the understanding of the mechanism by which suckling inhibits the release of pituitary LH and depresses the postovariectomy rise of plasma LH in lactating mammals. To that end, the effect of suckling (10 pups/animal) for 1 or 3 weeks on the LHRH content of the hypothalamus and preoptic area (POA) in ovariectomized and intact rats was examined. Controls consisted of intact and 1 or 3 week ovariectomized, nonlactating animals. Following decapitation, the brains were rapidly removed and blocks containing the POA and the hypothalamus (with median eminence) were isolated. Tissue was extracted with acetic acid and LHRH quantitated via validated RIAs utilizing 2 antisera specific for different portions of the LHRH molecule. Ovariectomy of nonlactating, diestrous animals resulted in a significant decline in hypothalamic LHRH, reaching 50% of control levels by 3 weeks. During the same intervals, plasma LH increased dramatically to 20- and 60-fold over intact controls by 1 and 3 weeks, respectively. In contrast, LHRH levels were not decreased at 1 or 3 weeks in ovariectomized rats which were suckled, at which time plasma LH was greatly depressed. When intact animals were evaluated, the suckling stimulus failed to induce a detectable change in LHRH content of the hypothalamus of LHRH in the POA between any of the treatment or control groups. These data from ovariectomized rats suggest that suckling inhibits LHRH release from the hypothalamus and hence provides an explanation for the depression of plasma LH observed in suckled ovariectomized and intact animals.
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PMID:Inhibition of the postovariectomy depletion of hypothalamic luteinizing hormone releasing hormone (LHRH) by suckling. 704 34

A discussion of the side effects of hormonal oral contraceptive (OC) use is presented. Studies show that the estrogen component of OCs works to suppress the release of GRH (gonadotropin-releasing hormone), reducing the serum FSH level. The gestagen component desensitizes the frontal lobe of the pituitary gland to the effect of GRH and suppresses the preovulatory LH peak. OCs can cause subjective side effects such as nausea, headache, depression, which can also be observed during placebo use. Breakthrough bleeding, spotting, silent menstruation, and post-pill amenorrhea are menstrual irregularities which can be linked to OC use; 98% of those who discontinue OC use show normal biphasic menstrual cycles 3 cycles after discontinuation. A constant increase in serum triglyceride levels, small increases in cholesterol and phospholipid levels are observed among OC users. Minor cases of hyperinsulinism are observed among OC users with no history of diabetes; glucose tolerance tests should be regularly administered to OC users who have a risk of diabetes or a history of pregnancy diabetes. Serum levels of proteins are affected by OC use, probably due to the effects of OC use on liver function. Studies have shown an increased risk of thromboembolism and circulatory disorders among OC users, especially those who are over 30 years of age or who smoke. OC use has been linked to development of benign tumors of the liver and the cervix. Gestagens appear to reduce the frequency of endometrial mitosis. Other medications, e.g. analgesics, barbituates, can reduce the effectiveness of OCs. For adolescents, sequence preparations are preferred and should be administered only after a 1 year period of regular menstruation. Thorough check-ups should be performed on OC users twice yearly, and contraindications should be scrupulously observed.
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PMID:[Effects and side effects of hormonal contraceptives]. 741 48


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