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)

Rats (200-260 g) were exposed in sealed, recycling chambers continuously for 2-30 days to gas mixtures designed to maintain the same alveolar PO2 in the presence or absence of inert gas. Mixtures with inert gas (N2, He, or Ne) were at ground level; those without inert gas (100 percent O2) were in an altitude chamber. The O2 categories were: I-100 percent O2 at 747 torr; II-74 percent O2 + 26 percent inert and 566 torr 100 percent O2; III-47 percent O2 + 53 percent inert and 381 torr 100 percent O2; IV-21 percent O2 + 79 percent inert and 197 torr 100 percent O2. One of the two room-air controls was "restricted-fed" to the level of the lowest intake group. Measurements included body, pituitary, and thyroid weight, food and water intake, plasma volume and hematocrit, pituitary and plasma TSH, and plasma PBI. Severe depression in all variables and over 50 percent mortality was seen in I by day 4. All variables were depressed in II, but there was no mortality to 20 days. Pituitary-thyroid function appeared to be particularly sensitive to depression by hyperoxia, with plasma TSH levels reduced between 42 and 60 percent in II and III. No effect was attributable to the inert gas, whether it was N2, He, or Ne, nor was any specific effect traceable to the presence or absence of inert gas.
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PMID:Pituitary-thyroid function of rats in hypobaric oxygen-inert gas environments. 80 43

Hypogonadal (hpg) mutant mice, with a congenital deficiency of hypothalamic gonadotrophin-releasing hormone (GnRH), and testicular feminized (tfm) mice, which lack a functional androgen receptor, were used to study the effects of the potent GnRH agonist 'Zoladex' (ICI 118630; D-Ser (Bu(t))6, Azgly10-GnRH) on pituitary and gonadal function. Zoladex (0.5 mg) in a sustained-release lactide-glycolide copolymer depot was administered subcutaneously under anaesthesia and was left in place for 7 days, after which time the effects of the drug upon pituitary and serum gonadotrophin concentrations, glycoprotein hormone subunit mRNAs and testicular morphology were investigated. At the pituitary level, Zoladex treatment resulted in a substantial reduction in LH content in normal males, and LH content was depressed in hpg mice even below the basal levels normally found in these mutants. Pituitary LH content in the Zoladex-treated animals was depressed in the tfm groups, but not to the same levels as those found in the normal and castrated normal mice. Zoladex treatment at the time of castration prevented the post-operative elevation in serum LH associated with castration alone. In the androgen-deficient tfm mouse, Zoladex did not depress the normally elevated serum LH levels. Serum LH in the hpg animals was, in all cases, below the limit of detection of the assay. Pituitary FSH content was depressed into the hpg range in both the normal and castrated animals, but there was no further depression in the hpg mice. The pituitary content was reduced in the tfm mice, again the effects not being as dramatic as in the normal and castrated animals. Serum FSH content, as measured by radioimmunoassay, was depressed by 50% in normal mice; there was no reduction in the hpg mice, however. With regard to pituitary gonadotrophic hormone gene expression, Zoladex administration to normal mice caused a dramatic reduction in LH beta mRNA content, to a level approximating that found in untreated hpg mice. The drug also depressed LH beta mRNA in the castrated group to the hpg range when given at the time of castration, whereas in untreated castrated mice there was a significant increase in LH beta mRNA. In the tfm mouse, which can be considered as a model for long-term failure of androgen feedback, Zoladex again induced a fall in LH beta mRNA, but not to the same extent as in the normal and normal castrated group. Zoladex had no effect on the already low levels of LH beta mRNA found in hpg mice.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of the gonadotrophin-releasing hormone agonist 'Zoladex' upon pituitary and gonadal function in hypogonadal (hpg) male mice: a comparison with normal male and testicular feminized (tfm) mice. 138 60

Stressors generally induce a depression of the hypothalamus-pituitary-testis (HPT) system, mediated by the activated hypothalamus-pituitary-adrenocortical (HPA) system, resulting in a fall in plasma luteinising hormone (LH) and testosterone levels. Hypothalamic gonadotrophin-releasing hormone (GnRH) secretion may be suppressed by endogenous opioid peptides (EOP) and/or corticosteroids. The latter dramatically enhance the negative feedback effects of testosterone on both the hypothalamus and pituitary. Pituitary gonadotrophin secretion may be reduced by adrenocorticotrophic hormone or by EOP of hypothalamic or pituitary origin. Decreases in plasma concentrations of testosterone, independent of gonadotrophins, can be induced by corticosteroids. These hormones might reduce the number of Leydig-cell LH-receptors or occupation of LH-receptors. Testicular steroidogenesis may also be inhibited by pro-opiomelanocortin-derived (opioid) peptides secreted by the Leydig cells. There are some indications of increases in LH and testosterone during acute stress and, in dominant male animals, during the stress of social conflict. The latter finding indicates a difference in stress response between dominant and subordinate males. In subordinate males, decreased feedback sensitivity may allow hypersecretion throughout the HPA system. As a result, corticotrophin releasing hormone may induce the release of EOP from the hypothalamus, which inhibit the HPT axis. This inhibition may be enhanced by a corticosteroid-induced decrease in testosterone feedback.
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PMID:Stress and the endocrine hypothalamus-pituitary-testis system: a review. 188 89

Fifty-six patients with acromegaly were treated with external irradiation, 50 Gy, after unsuccessful pituitary surgery. A 50% reduction of pre-irradiation growth hormone levels was obtained in 51/56 patients. This level was reached after 26 +/- 14 months in 33 patients with prolactin levels less than 25 micrograms/l at diagnosis, after 21 +/- 17 months in 18 patients with prolactin greater than or equal to 25 micrograms/l, and after 20 +/- 21 months in 12 patients with prolactin greater than 40 micrograms/l at diagnosis. A further 50% decrease of growth hormone levels was obtained in 40/51 patients 42 +/- 22 months after radiotherapy, indicating that in clearly responsive patients, the growth hormone depression after radiotherapy follows a first order reaction. Four patients did not reach a 50% reduction of growth hormone levels 48-80 months after radiotherapy. During 10 years of follow-up, the growth hormone depression tended to be more pronounced in patients with mixed secretion of growth hormone and prolactin. The reduction of growth hormone levels was not correlated with the irradiated volume or the cumulative radiation effect. Within the first year, prolactin increased within the normal range in normoprolactinemic patients and remained so during follow-up. In hyperprolactinemic patients, prolactin decreased successively but to a lesser extent than growth hormone. Pituitary insufficiencies increased over time and three patients developed GH-insufficiency. Hypothalamic damage as indicated by prolactin changes was a regular phenomenon after radiotherapy.
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PMID:External irradiation of growth hormone producing pituitary adenomas: prolactin as a marker of hypothalamic and pituitary effects. 200 40

Transplantation of brain tissue has been used to ameliorate the genetic lesion of the hypogonadal mutant mouse. This animal does not synthesize gonadotropin-releasing hormone (GnRH) and so has an infantile reproductive system. Implantation of normal fetal or neonatal preoptic area containing GnRH neurons reverses many aspects of the reproductive deficiency. Pituitary and plasma levels of gonadotropins rise, followed by growth of the gonads and sexual organs. Pituitary release of gonadotropins is episodic, suggesting that the grafted tissue is integrated into the "pulse generator." The vast majority of grafted animals do not show castration-induced elevations of luteinizing hormone (LH) nor respond to exogenous steroids with a depression in circulating LH. Negative feedback of gonadal steroids seems to be inoperative. In contrast, some females can show ovulatory surges of LH in response to mating (reflex ovulation), after administration of exogenous steroid (progesterone), and, on rare occasion, ovulation cycles occur spontaneously. Anatomical studies demonstrate that reproductive recovery is dependent on the outgrowth of GnRH axons to the host median eminence. Some but not all of the GnRH neurons within the grafts contribute to this innervation. GnRH axons exit into the host along well-defined pathways, recapitulating in part the paths taken by normal axons. How the graft and host are integrated to produce the panoply of reproductive responses is the subject of current study.
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PMID:Repair of reproductive deficits by neural transplantation. 217

Rapid and prolonged effects of recombinant human interleukin-1 alpha (IL-1 alpha) on mouse thyroid were studied. After daily administration of 15 micrograms or 1 microgram IL-1 for 7 consecutive days, serum T4 concentrations rapidly fell to undetectable levels but returned to near control level after the cessation of IL-1. On the 31st day, 3 weeks after the drug cessation, a significant depression of serum T4 was observed again. In addition, the IL-1-treated mouse thyroid showed an in vitro unresponsiveness to TSH, with an increase of pituitary TSH (2.24-fold by 15 micrograms IL-1). To understand underlying mechanisms further, serial observations were performed. Thyroidal T4 contents increased initially, decreased to a low level at day 14, and returned to approximately the control level. IL-1 administration induced an increase in the basal thyroidal cAMP level for a prolonged period. Its response to TSH showed a gradual decline to a level approximately 30% of the control by the 31st day. Pituitary TSH contents on the 22nd and 31st days showed significant elevations. Slight decreases in thyroidal TSH binding and T4 contents also were seen concomitantly. These studies indicate that an administration of a large dose of IL-1 results in a dramatic decrease in serum T4 primarily through the inhibition of T4 release from the thyroid. The results also indicate the induction of a prolonged hypothyroid state due to the unresponsiveness to TSH via a postreceptor mechanism.
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PMID:Prolonged effects of recombinant human interleukin-1 alpha on mouse thyroid function. 222 18

In order to find the correlation between dexamethasone suppression test (DST) and TSH response to TRH in the differential diagnosis of subtypes of depression, and to evaluate the possible relationship between Hypothalamic-Pituitary-Adreno-cortisol axis, Hypothalamic-Pituitary-Thyroid axis function, psychopathological symptoms, and the possible influence of age and sex, 107 depressed patients were studied. The relationship between both tests (DST and THS response to TRH) and the subtypes of depression was unspecific. The results did not show psychopathologic differences between depression subgroups. DST appeared to be a good marker for the "state" of illness, whereas TSH was better as a predictor for the outcome.
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PMID:[Usefulness of neuroendocrine function tests in the differential diagnosis of depression]. 251 35

Male Syrian hamsters were kept under either 14 h light/10 h dark (lights on at 06.30 h) or 2 h light/22 h dark (lights on at 14.30 h) photoperiods. Groups of hamsters under each photoperiod were rendered hypothyroid by addition of 0.4% thiourea to the drinking water. These hamsters received, in addition, either a daily evening injection of saline or a daily injection of 25 micrograms melatonin in saline. Groups of intact controls and pinealectomized control hamsters were also maintained under the two photoperiodic conditions. After 10 weeks under the different conditions the hamsters were killed by decapitation, and serum samples assayed for thyroxin, thyroid-stimulating hormone (TSH), and prolactin (PRL). Pituitary extracts were assayed for TSH and PRL. Hypothyroidism in hamsters receiving thiourea was confirmed by radio-immunoassay data showing low serum thyroxin and greatly elevated serum TSH concentrations. Melatonin injections resulted in significant depression of serum TSH in thiourea-treated hamsters under short photoperiod compared to saline-injected controls. Both melatonin injections and short photoperiod resulted in a significant reduction of pituitary TSH in hamsters on thiourea compared to values obtained from similarly treated animals under the 14 h light/10 h dark photoperiod. Hypothalamic concentrations of thyrotropin-releasing hormone (TRH) were significantly elevated by melatonin injections and by short photoperiodic conditions, but not by thiourea administration. The short photoperiod resulted in testicular involution which was completely reversed by pinealectomy and partially reversed (to 53% of controls) by thiourea treatment. Involution of gonads was complete in thiourea-treated animals under short photoperiod, if they received melatonin injections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of afternoon injections of melatonin in hypothyroid male Syrian hamsters. 308 89

Pituitary glands of proestrous (PRO) rats display enhanced LH secretory response to LHRH when compared to pituitary glands of estrous (EST) rats. In addition proestrous pituitary glands display a self-potentiating (priming) response to LHRH, whereas estrous pituitary glands do not. This study addresses the role of the proestrous surge of progesterone in converting the proestrous-like LH secretory responses of the pituitary gland to those of estrus. Anterior pituitary glands were obtained from PRO and EST rats. In addition, Pro rats were treated with pentobarbital alone (PRO/PB) or with pentobarbital plus progesterone (PRO/PB-P4). Pentobarbital was given to prevent proestrous surges of LH and progesterone. Pentobarbital-treated animals were killed the day after treatment, estrus. Pituitary glands from each group were tested for LH secretory response in a superfusion chamber with exposure of two 15-min pulses of 10 nM LHRH separated by 90 min, or assayed for LHRH receptor content using iodinated D-Ala6-LHRH. Anterior pituitary glands from PRO rats secreted higher levels of LH than EST rats in response to an LHRH pulse. Only PRO anterior pituitary glands secreted priming responses to LHRH. Though anterior pituitary glands obtained from pentobarbital-treated rats showed LH responses of similar magnitude to anterior pituitary glands of PRO rats after initial LHRH challenge, they did not display priming responses. Progesterone replacement (PRO/PB-P4) led to depressed secretory responses when compared to PRO pituitary glands similar to EST rats. LHRH receptor concentrations in pituitary glands of EST rats was lower than those in pituitary glands of PRO rats. Depression of pituitary LHRH receptor concentration from proestrus to estrus was prevented by pentobarbital-treatment on proestrus. Estrus-like depression of receptor concentration was restored after progesterone treatment (PRO/PB-P4). These data suggest the LHRH receptor depression on estrus is a consequence of the secretion of progesterone on proestrus. Further, the declining magnitude of the in vitro LH-secretory response to LHRH follows a declining LHRH receptor concentration; however no correlation exists between receptor number and ability to prime.
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PMID:Secretion of luteinizing hormone (LH) and pituitary receptors for LH-releasing hormone as modified by the proestrous surge of progesterone. 609 51

In the present work the effects of oestradiol benzoate (EB) on pituitary and plasma concentrations of TSH, plasma T4 and T3, and thyroidal activity of male and female rats have been studied. Wistar rats weighing between 150 to 200 g were injected sc with varying doses of EB in corn oil for 9 or 30 days. The animals were exsanguinated by cardiac puncture and the hypophyses removed and individually homogenized at 4 degrees C in 200 microliters PBS buffer. Pituitary and plasma TSH were measured by radioimmunoassay. Thyroidal activity was evaluated by a 4 h 131I uptake and by 48 h thyroidal release plasma slopes derived form the ratio PB[125I] (from thyroidal secretion) to PB[131I] (from exogenous [131I]T4). In both male and female rats the 10 and 25 micrograms doses of EB produced a significant decrease in pituitary TSH content; this effect was more pronounced when the 25 micrograms dose was given over 30 days. Plasma T4 decreased significantly; plasma T3 was moderately elevated in all groups (NS) and significantly increased in female rats treated with 25 micrograms EB (P less than 0.01). It is concluded that EB induced a marked depression of intrapituitary TSH, probably due to a decrease in synthesis, without affecting the release of TSH into the circulation. Moreover, EB accelerated peripheral T4 kinetics and thyroid gland activity, albeit to a moderate degree.
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PMID:Effects of oestradiol benzoate on the pituitary-thyroid axis of male and female rats. 682 63


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