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)

Pituitary-adrenal activity was evaluated with the dexamethasone suppression test in 11 patients over their multiple hospitalizations for major depression. All six patients who were suppressors during their index admission had one subsequent admission over the period of study during which they were again suppressors. Of five patients who were nonsuppressors during their index admission, three had one subsequent admission and two had three subsequent admissions. Four of these patients were again nonsuppressors during a subsequent admission. For patients who were nonsuppressors during some but not all admissions for depression, pituitary-adrenal activity appeared related to the persistence of the depressive episodes.
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PMID:Pituitary-adrenal regulation over multiple depressive episodes. 696 34

Male rats (25-26 days of age) housed with 14 hours of light per day (lights on 0600--2000 hours) were either olfactory bulbectomized (rendering them anosmic), bulbectomized plus pinealectomized (Pinx), or left intact. On the day following the operations, intact, anosmic, and anosmic-Pinx animals began receiving single, daily afternoon (1700--1800 hours) subcutaneous injections of 50 microgram of melatonin (MEL) for six weeks, while an additional group of intact controls received injections of diluent. At the end of this period, body, anterior pituitary, testicular, and seminal vesicle weights were significantly reduced in intact-MEL-treated animals. Anosmic animals that had been treated with MEL experienced a further, highly significant, 65%, 90%, and 85% depression in testicular, seminal vesicle, and ventral prostate weights, respectively, as compared with intact control and MEL-treated rats. Additionally, both body and anterior pituitary weights were significantly decreased in MEL-treated, anosmic rats. Anosmic-Pinx rats treated with MEL had organ and body weights that were intermediate between those of intact-MEL and anosmic-MEL-treated animals. Pituitary and serum levels of prolactin (Prl) were significantly lower in anosmic-MEL-treated rats than in intact-MEL-treated groups. Similarly, Prl levels were depressed in the anosmic-Pinx rats treated with MEL; however, serum Prl was not statistically lower than in intact or intact-MEL-treated animals. These results indicate that anosmic male rats have an increased sensitivity to antigonadotrophic and Prl-inhibitory effects of MEL. Futhermore, the data suggest that the presence of the pineal gland in anosmic rats is important in permitting anosmia maximally to sensitize the neuroendocrine-reproductive axis to the antigonadotrophic effects of exogenously administered MEL.
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PMID:An interaction between the pineal gland and olfactory deprivation in potentiating the effects of melatonin on gonads, accessory sex organs, and prolactin in male rats. 740 Nov 93

Exposure of male rats to ozone for 24 hrs at 1 ppm caused a profound depression of the pituitary-thyroid axis as indicated by a highly significant reduction of circulating thyrotropin hormone (TSH), thyroid hormones (T4 and T3), and protein-bound iodine (PBI). The metabolic clearance of TSH was not altered during ozone exposure and the high TSH levels seen in thyroidectomized rats were also not affected. Circulating prolactin (PRL) levels were significantly elevated after exposure. Pituitary TSH and PRL content was considerably increased in ozone-exposed rats; however, only TSH was released significantly above control values in vitro. Thyroid weight was also significantly increased after exposure. The results suggest that the depression of the pituitary-thyroid axis may be an adaptive mechanism during ozone exposure by reducing hypothalamic stimulation via thyrotropin releasing hormone (TRH) and at the same time lifting the hypothalamic catecholamine inhibition on PRL release. Both may be necessary alterations in order to develop tolerance during ozone exposure.
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PMID:Changes in thyroid function after short-term ozone exposure in rats. 744 Nov 19

Although plasma levels of Met-enkephalin and beta-endorphin are elevated in patients suffering from liver failure, it is not known whether central nervous system (CNS) opioidergic neurotransmission is altered in these patients. Such changes may contribute to the motor dysfunction, psychiatric abnormalities and CNS depression observed in hepatic encephalopathy (HE). Therefore, Met- and Leu-enkephalin, dynorphin A and beta-endorphin levels were measured in discrete brain regions and plasma from thioacetamide-treated rats in Stages II to IV of HE. Pituitary and plasma beta-endorphin, Met- and Leu-enkephalin concentrations increased with the severity of HE by 50 to 290%. Pituitary and brainstem dynorphin A levels increased whereas plasma levels decreased in rats with thioacetamide-induced fulminant hepatic failure. Both striatal Met- and Leu-enkephalin levels increased and hypothalamic concentrations decreased in HE. Concurrent with the increase in striatal Met-enkephalin levels was a 26 to 48% decrease in the density of striatal and hypothalamic delta receptors. No change in either the density or affinity of radioligand binding to mu or delta receptors was observed in the CNS. Finally, administering (+/-)-naloxone (5 and 10 mg/kg) or (+/-)-naltrexone (5-15 mg/kg), but not (+)-naloxone (10 mg/kg), significantly increased the motor activity of rats with Stage III HE. Whereas elevated plasma levels of opioid peptides may play a role in the peripheral manifestations of hepatic failure (ascites and hypotension), increased CNS levels of these peptides may be involved in the neuropsychiatric abnormalities characteristic of HE. Thus, opioid antagonists may be effective in ameliorating some of the neurological manifestations of HE.
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PMID:Brain and plasma levels of opioid peptides are altered in rats with thioacetamide-induced fulminant hepatic failure: implications for the treatment of hepatic encephalopathy with opioid antagonists. 771 65

Removal of the pups results in an abrupt and marked depression in plasma prolactin (PRL) level of the lactating mother. The present studies were undertaken to investigate what kind of sensory input (smell, sound, visual, touch etc.) from the pups is essential for the mother to avoid the pituitary PRL response to pup-removal. Therefore, various partial separations were made and their effect on plasma PRL levels tested: a. The pups were placed into a small glass having holes on its cover; b. they were put into a long measuring tube not covered; c. the pups were placed into the feeding trough made of a wireframe; d. a dividing wall made of glass or metal was slowly let down when the mother spontaneously went away from her pups; e. the nipples were covered by a cotton plaster. Pituitary PRL responses were almost identical after all these separations and similar to that one obtained after removal of the pups from the cage. In addition, separation of the mother resulted in a rise in plasma corticosterone concentrations. The findings suggest that the pup-removal induced inhibition of PRL secretion is a very complex event for the mother and cannot be prevented by partial separations when the mother can see, smell her pups, or hear them or even can touch them with her nose. We assume that separation of the pups is a stress for the mother and cannot simply be due to the lack of just one kind of sensory input from the pups. This assumption is in line with our recent observations indicating that in lactating rat stress causes a decrease in plasma PRL level.
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PMID:Effect of various partial separations of the litters from their mother on plasma prolactin levels of lactating rats. 772 15

Pituitary adenylate cyclase activating polypeptide (PACAP) is a novel vasoactive intestinal peptide (VIP)-like peptide isolated from ovine hypothalami. The presence of PACAP-like immunoreactivity was recently demonstrated in nerve cell bodies of sensory ganglia in the rat. Since PACAP belongs to a large family of chemically related neuropeptides, we have, in the present study, tried to establish the synthesis of PACAP in neurons of sensory ganglia, using in situ hybridization with a 35S-labelled oligonucleotide probe complementary to PACAP mRNA. The expression of PACAP was compared to that of calcitonin gene-related peptide (CGRP) using a radiolabelled CGRP oligonucleotide probe. The PACAP probe labelled small to medium-sized neurons in the trigeminal ganglion and dorsal root ganglia at different levels, indicating the presence of PACAP mRNA. The CGRP probe labelled nerve cell bodies of varying size, outnumbering those labelled by the PACAP probe. In dorsal root ganglia, cells expressing PACAP constituted c. 10% and those expressing CGRP 46% of the total number of nerve cell bodies. Expression of PACAP was seen in a small subpopulation of cells expressing CGRP. We conclude that PACAP is synthesized in a subpopulation of neurons of sensory ganglia in the rat. Therefore, the recently described effects of PACAP--cutaneous vasodilation, potentiation of oedema formation and depression of nociceptive spinal reflexes--may be physiological and related to neurogenic inflammation and modulation of pain transmission.
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PMID:Pituitary adenylate cyclase activating polypeptide expression in sensory neurons. 789 55

The effects of daily administration of phenobarbitone on the mitotic rates of several tissues were investigated by bromodeoxyuridine (BrdU) immunocytochemistry. Phenobarbitone (80 mg/kg per day) was dosed to AP Wistar male rats for up to 7 days and BrdU (10 mg/ml) was given by infusion at a rate of 10 microliters/h via subcutaneously implanted osmotic minipumps for 2 days prior to necropsy on days 1, 2, 3, 5 and 7. BrdU-labelled nuclei were visualised by peroxidase-antiperoxidase immunocytochemistry and counts of the numbers of labelled cells (labelling index, LI%) made from at least 1000 cells per tissue section(s). The LIs of several tissues (testis, adrenal cortex and medulla, kidney distal convoluted tubule and exocrine pancreas) showed no statistical difference by comparison with controls. Several tissues exhibited characteristic responses to phenobarbitone administration. Pituitary and endocrine pancreas LIs were decreased while those of thyroid, liver and kidney proximal convoluted tubule were increased. The pattern of LI increase was unique to each tissue with liver (median and lateral lobes) increased two-fold on day 3 and returning to control levels thereafter while kidney proximal tubule LI rose gradually with time and remained elevated on day 7. Thyroid LI on day 1 was almost double that of day 0 control and increased steadily thereafter. These data illustrate the varied responses of different tissues to phenobarbitone exposure, namely, depression and stimulation of mitosis. The causation of these functional changes is discussed in relation to direct and indirect effects on functional parameters, especially enzyme induction, alterations in hormonal and growth factor status and receptor regulation.
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PMID:Assessment of the influence of subacute phenobarbitone administration on multi-tissue cell proliferation in the rat using bromodeoxyuridine immunocytochemistry. 831 89

The differential regulation of immunoactive FSH and LH secretion by endogenous LH-RH was studied using LH-RH antagonists (Ac-D-Trp1,2, D-Cpa2, D-Lys6, D-Ala10LH-RH (MI-1544) and (Ac-D-Nal1, D-Phe(pCl2), D- Trp3, D-Cit6, D-Ala10LH-RH (SB-030) in ovariectomized (OVX) and regularly cycling rats. Single injections of 10 micrograms and 100 micrograms doses and long-term treatment with 10 micrograms doses of MI-1544 were used in OVX animals. Serum and pituitary LH and FSH, as well as serum estradiol and progesterone was determined by RIA during and/or after the treatment. Single injections of MI-1544 in OVX animals caused prompt (in 2 h) and long-lasting (for more than 24 h) suppression of the serum LH, while no or late decrease (after more than 6 h) of the serum FSH. Long-term treatment with the same analog decreased the serum LH (by 50%) and moderately increased the pituitary LH (by 21%) but did not change the serum and the pituitary FSH concentrations. In normal rats, long-term treatment with both of our analogs also resulted in divergent alterations in the LH and FSH concentrations. Serum LH dropped to undetectable levels,while serum FSH did not change significantly. Pituitary LH increased (by 31 to 41%), while FSH decreased (by 27 to 38%). Marked depression was found in the serum progesterone (by 64%) but no significant change in the serum estradiol levels, after the long-term treatment for 21 days. The ovarian cycles were interrupted, and no ovulation appeared during the treatment. Significant decrease was detectable in the weight of the ovaries (by 46%), whereas the weight of the uteri did not change or slightly elevated (by 22%), after the treatment with SB-030 or MI-1544, respectively.
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PMID:Antiovulatory doses of antagonists of LH-RH inhibit LH and progesterone but not FSH and estradiol release. 868 Apr 31

There have been few reports of factitious Cushing syndrome. To characterize the clinical and laboratory features leading to this unusual diagnosis, we describe 6 patients (5 women, 1 man), ages 31-44, identified retrospectively among 860 patients evaluated for hypercortisolism at the National Institutes of Health Clinical Center. All six patients had multiple surgeries unrelated to Cushing syndrome and a history of depression or anxiety. Four patients had close contact with the medical profession, three a history of drug abuse, and three had undergone previous treatment for Cushing syndrome. The physical features of Cushing syndrome were variable and not helpful in the differential diagnosis with endogenous Cushing syndrome. Four patients had striking variability in urine-free cortisol (UFC) and 17-hydroxysteroid (17-OHCS) values from low to high. Adrenal computed tomography, performed in two patients, showed small adrenal glands (n = 1) or a left-sided mass (n = 1), and adrenal magnetic resonance imaging, performed in one patient, showed atrophic glands. Pituitary magnetic resonance imaging, carried out in four patients, was either normal (n = 1) or exhibited questionable signs of microadenoma (n = 3). Determination of synthetic glucocorticoids by high pressure liquid chromatography (HPLC) was positive in the four patients in whom it was performed. Factitious Cushing syndrome is a difficult diagnosis. To conserve time and resources, high pressure liquid chromatography analysis of urine steroids, the most definitive test for the factitious disorder, should be performed whenever there is clinical suspicion of glucocorticoid abuse.
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PMID:Factitious Cushing syndrome. 885 3

Raised activity of the LH axis caused by activating mutations of LH receptor gene presents with precocious puberty in boys, analogous to the presentation of LH secreting pituitary adenomas (Faggiano et al., 1983; Ambrosi et al., 1990). LH "hyperactivity' in females appears to have no effect. Hyperactivity of the FSH axis caused by activating mutations of the FSH receptor gene might parallel the presentation of FSH secreting pituitary adenomas with Sertoli cell hypertrophy in men (Heseltine et al., 1989) or reversible premature ovarian failure in women (Moses et al., 1986; Okuda et al., 1989). Indeed the first such case to be described is a male who maintained testicular volume and fertility in the absence of gonadotrophins (Gromoll et al., 1996). Female precocious puberty may require hyperactivity of both gonadotrophin axes because of the "two-cell' arrangement required for ovarian oestrogen production. Mutations of the Gs alpha-subunit gene can mimic this situation in some women with the McCune-Albright syndrome (Malchoff et al., 1994). Lack of LH activity caused by defects in the LH beta molecule causes infertility in men and that resulting from inactivating mutations of the LH receptor gene causes Leydig cell agenesis in men while ovarian development in females is relatively normal. Lack of FSH activity caused by defects in the FSH beta caused infertility in a female, and that caused by inactivating mutations of the FSH receptor gene causes ovarian dysgenesis in women but only variable depression of spermatogenesis in men. Incidentally, this categorization of reproductive disorders may also be applied to the TSH axis. Pituitary adenomas and activating mutations of the TSH receptor gene (Parma et al., 1993) cause hyperthyroidism and TSH beta gene defects (Hayashizaki et al., 1989) and inactivating mutations of the TSH receptor gene (Sunthornthepvarakul et al., 1995) cause hypothyroidism. To complete the analogy with thyroid disorders, it is curious that despite structural similarities with the TSH receptor, neither LH nor FSH receptor autoantibodies have a prominent role in ovarian pathophysiology (Moncayo et al., 1989; Van Weissenbruch et al., 1991; Simoni et al., 1993). Complete gonadotrophin resistance is likely to be very rare, however, so what are we likely to find in partial gonadotrophin resistance? Might the "resistant ovary syndrome' come right in the end, with corresponding minor FSH receptor mutations? Experience with insulin and androgen resistance syndromes suggests that such a scenario is unlikely. Insulin receptor gene mutations are found in extreme Type A insulin resistance but not in moderate forms of insulin resistance (O'Rahilly et al., 1991). Androgen receptor gene mutations are found in nearly all cases of complete androgen insensitivity but rarely in partial forms (Patterson et al., 1994). Mild resistance to hormone action is rarely detectable in relatives who are heterozygous for receptor mutations which are inherited in a recessive pattern. It seems unlikely therefore, that individuals heterozygous for inactivating receptor mutations will manifest symptoms of reproductive disorders and account for common conditions. Thus, while mutation analysis provides new insights into the gender specific role of the gonadotrophins the cause of early gonadal failure in the majority of individuals remains a mystery.
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PMID:Clinical manifestations of genetic defects affecting gonadotrophins and their receptors. 903 30


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