Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conditioned taste aversion for a 5% glucose solution (sugar water) was induced in rats by an i.p. injection of LiCl 30 min after the first presentation of sugar water. Extinction of conditioned taste aversion was measured either in the forced-drinking test or in the preference-drinking test. In the forced-drinking test sugar water was the only fluid presented to the animals during extinction sessions. In the preference-drinking test the animals had the choice of tap water or sugar water. The rate of extinction was much slower in the preference test. The ACTH-analogues, ACTH 4-10 and ACTH 4-10 7d Phe, and alpha-MSH delayed extinction in the preference test but not extinction in the forced-drinking test. ACTH 11-24 was without any effect. MSH-release inhibiting factor (MIF) facilitated extinction in the forced-drinking test but did not alter extinction in the preference test. The peptides did not affect intake of tap water of preference of sugar water over tap water by control rats.
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PMID:Hormonal influences of the extinction of conditioned taste aversion. 0 99

Quantitative receptor autoradiography using Bolton-Hunter iodinated substance P (SP) was used to localize specific sites in the rat hypothalamus. The amount of SP and neurokinin A (NkA) in extracts from discrete areas of the hypothalamus was measured using specific radioimmunoassays. A high density of SP binding sites was observed in the perimeter of the magnocellular paraventricular and supraoptic nuclei, while the magnocellular nuclei themselves possessed a low receptor density. In control animals, the number of SP binding sites was also low in the arcuate nucleus and the median eminence. Substance P and NkA peptide concentrations were highest in the paraventricular nucleus (PVN), decreasing in the following order: arcuate nucleus (Arc) greater than median eminence (ME) greater than supraoptic nucleus (SON) greater than subfornical organ (SFO). In animals given 340 mmol/l NaCl instead of tap water to drink for 12 days, significant increases in the number of SP binding sites occurred in the medial parvocellular subdivision of the PVN, periamygdaloid cortex, medial preoptic nucleus, Arc, and ME, but other hypothalamic areas were unaffected. In saline-treated animals, significant increases in SP and NkA peptide concentrations were observed in the ME, while in the SFO only the concentration of NkA increased significantly. In the SON, substance P and neurokinin A levels were doubled, whereas in the PVN and Arc no changes in peptide levels were observed. Chronic osmotic stimulation is associated with lowered circulating levels of adrenocorticotropin releasing hormone (ACTH), and the present data further substantiate the hypothesis that hypothalamic tachykinin-containing neuronal terminals are centrally involved in the inhibition of anterior pituitary ACTH release observed during chronic osmotic stimulation.
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PMID:Osmotic regulation of substance P and neurokinin A peptide content and substance P binding sites in distinct hypothalamic nuclei of the rat. 127 30

This study demonstrates that a chronic osmotic stimulus can influence the hypothalamo-pituitary axis by inhibiting the secretion of basal and adrenalectomy-elevated adrenocorticotropin (ACTH) from the anterior pituitary. In rats given 340 mM NaCl instead of tap water to drink for 12 days, plasma concentrations of ACTH decreased to 105 +/- 27 pM (mean +/- S.E.M., n = 6) compared with control animals (182 +/- 13 pM). In adrenalectomised (ADX) rats given 150 mM NaCl to drink for 12 days, plasma ACTH concentrations were greatly increased (783 +/- 141 pM) but in ADX rats treated with 340 mM NaCl for the same period, plasma ACTH was similar to controls (237 +/- 59 pM). The corticotropin-releasing factor (CRF-41) content of the median eminence (ME) was reduced in ADX rats on 150 mM NaCl (854 +/- 78 fmol) and further reduced in ADX rats given 340 mM NaCl (510 +/- 56 fmol) compared with control animals (1239 +/- 114 fmol), suggesting that the decrease in plasma ACTH concentrations in saline-treated animals is secondary to a decrease in the secretion of CRF-41 from the ME. These data are the first evidence for a central mechanism, independent of glucocorticoid feedback, through which a chronic osmotic stimulus can inhibit the activity of CRF-41 neurons.
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PMID:Inhibition of rat corticotropin-releasing factor and adrenocorticotropin secretion by an osmotic stimulus. 216 61

Different hormones of the hypothalamo-pituitary-adrenal axis (corticotropin-releasing factor, adrenocorticotropic hormone, corticosterone) were measured in brain pieces (stalk, median eminence, hypothalamus), hypophyses, adrenals and plasma of 21-day-old rat fetuses from mothers which were given either plain tap water or water containing dexamethasone acetate (10 micrograms/ml) from day 15 to 21 of gestation. Dexamethasone induced drastic reduction of body weight (-66% vs. controls), severe atrophy of the adrenals (-83%) and a sharp drop in their corticosterone content (-74%). Fetal plasma corticosterone levels were below the lower limit of detection of the competitive corticosteroid-binding globulin (CBG) radioassay (less than 0.01 microgram/ml). Both atrophy and severe reduction of the adrenal activity in fetuses from dexamethasone-treated females were in good correlation with a drastic decrease in plasma adrenocorticotropic hormone (ACTH) levels which were below the lower limit of detection of the radioimmunoassay (RIA) used (less than 10 pg/ml) and a significant reduction in pituitary ACTH content (-93%). The low corticostimulating activity of the fetal hypophyses was associated with a drop in both corticotropin-releasing factor (CRF) hypothalamic content (-57%) and concentration (-67%). The effects of dexamethasone on plasma and pituitary ACTH concentrations in 21-day-old fetuses were compared to those, previously reported, of encephalectomy and decapitation performed on day 16 of gestation. The reported data were consistent with the present results, suggesting both pituitary and hypothalamic sites for the in vivo inhibiting action of dexamethasone on the rat hypothalamic-pituitary-adrenal axis in late gestation.
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PMID:Effects of chronic maternal dexamethasone treatment on the hormones of the hypothalamo-pituitary-adrenal axis in the rat fetus. 282 15

Beta-endorphin concentrations were determined in the cerebrospinal fluid and blood before and after lumbar tap in 19 patients with lumbosacral pains. No statistically significant difference was observed in this concentration before and after lumbar tap, although in individual cases a significant rise of beta-endorphin occurred. The mean beta-endorphin concentration in blood was about twice as high as in the cerebrospinal fluid. No correlation was noticed between the concentration of beta-endorphin in blood and in CSF.
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PMID:[Beta-endorphin levels in the blood and cerebrospinal fluid in humans]. 293 69

Chronic treatment of rats with 15% (vol/vol) ethanol in tap water as their only source of liquid over a period of 3 weeks resulted in a strong decrease by almost 50% in tissue levels and in vitro release of immunoreactive beta-endorphin of the neurointermediate pituitary. Moreover, the in vitro incorporation of [3H]phenylalanine into peptides of the neurointermediate pituitary, immunoprecipitable with beta-endorphin antiserum, was found to be decreased by more than 30%. Analysis of beta-endorphin-related peptides on sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that chronic ethanol treatment reduced the in vitro biosynthesis of the beta-endorphin precursor pro-opiomelanocortin. This ethanol-induced effect was combined with a retardation in the time course of the posttranslational processing of the precursor into beta-endorphin. Thus, chronic ethanol treatment may influence the activity of enzymes which process the opioid peptide precursor pro-opiomelanocortin, leading to a decreased formation of the final secretory product beta-endorphin.
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PMID:Effects of chronic ethanol treatment on the in vitro biosynthesis of pro-opiomelanocortin and its posttranslational processing to beta-endorphin in the intermediate lobe of the rat pituitary. 608 35

Chronic implantation of a stimulating electrode in the thalamic relay nucleus (11 cases), in the periaqueductal gray (1 case) and in the internal capsule (2 cases) was performed in fourteen cases which suffered from intractable pain. All these cases could get pain relief at least initial two months. Ventricular fluids were collected before and after stimulation with optimal combination of parameters, and measurements of beta-endorphin were performed by radio-immunoassay. Intrathecal morphine (1mg) injection was performed in eight cases. Cerebrospinal fluids were collected by lumbar tap before and 24 hours after morphine injection. beta-endorphin immunoreactivity was measured by the same method. Pain relief was judged to be excellent if the patient so claimed, and if he discontinued analgesics. Pain relief was thought to be good when it was not completely controllable by stimulation but was sufficiently improved that the patient could do without analgesics. It was thought to be fair when patient could not discontinue analgesics, and poor when patient could not get pain relief. We usually attempt to prevent the stimulation-tolerance by administration of the monoamine precursors , i.e., 1-dopa and 1-tryptophan, on the basis of the experimental observation reported previously. In somatogenic pain patients, the thalamic relay nucleus stimulation was performed in 7 cases (excellent; 3, good; 1, fair; 3) and the periaqueductal gray stimulation in one case (good).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Thalamic relay nucleus stimulation for relief of intractable pain. Clinical results and beta-endorphin immunoreactivity in cerebrospinal fluid]. 633 Jun

Corticotropin releasing factor (CRF) reduces food intake in rats after central administration. In these studies we examined whether the adrenal gland and the vagus were involved in CRF suppression of intake. One hour intake was reduced by a 5 micrograms (ICV) injection of CRF in sham but not adrenalectomized rats maintained on 0.9% NaCl. In a separate experiment on rats maintained on tap water, the inhibitory effect of CRF (5 micrograms) lasted at least 4 hours in sham rats whereas adrenalectomized rats did not significantly differ from controls. These experiments suggest that the adrenal gland modulates the feeding response to CRF. As replacement with corticosterone (0.75 mg/kg) in total adrenalectomized rats did not restore responsiveness to 5 or 10 micrograms of CRF, we next studied whether the adrenal medulla was responsible for the decreased responsiveness to CRF. In rats lacking the adrenal medulla only, food intake was reduced by a 5 microgram injection of CRF; in sham rats, intake was significantly reduced by doses as low as 0.1 microgram of CRF. An additional experiment examined the effect of gastric vagotomy on the CRF feeding response. Vagotomized rats were as responsive to 5 and 10 microgram injections of CRF as sham rats, which suggests that the effect is not dependent on the vagus nerve. These findings indicate that the adrenal gland, primarily the medulla, plays an intermediate role in the reduction of food intake caused by central injections of CRF. This conclusion is consistent with the known effect of CRF on adrenomedullary discharge.
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PMID:Adrenal modulation of the inhibitory effect of corticotropin releasing factor on feeding. 660 18

Possibility of the development of clonidine-tolerance in the peripheral nervous tissue was examined using vas deferens isolated from rats chronically treated with clonidine. Rats were treated with clonidine for 10 days by adding the drug to drinking water (10 microgram/ml). For the control rats, drug-free tap water was provided. Electrically evoked twitch response of vas deferens was suppressed by adenosine, beta-endorphine and alpha 2-adrenergic agonists, such as clonidine and B-HT 933, both in control and clonidine-treated groups. Vas deferens isolated from clonidine-treated rats showed significantly lower responsiveness to the inhibitory effects of clonidine and B-HT 933 compared to those from control rats. Vas deferens from clonidine-treated rats also was less responsive to adenosine and beta-endorphin, both of which interact with presynaptic inhibitory receptors other than alpha 2-adrenoceptors. On the other hand, responsiveness of the postsynaptic smooth muscle to both alpha-adrenergic and muscarinic cholinergic stimulation did not change after 10 days of treatment with clonidine. These results suggest that clonidinetolerance can be induced in the peripheral nervous system by chronic treatment of this drug and that the tolerance is not specific to alpha 2-adrenergic agonists. Some common pathway in the inhibitory mechanisms of various agents or possible interactions between the different types of presynaptic inhibitory receptors may be involved in this phenomenon.
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PMID:Development of clonidine-tolerance in the rat vas deferens: cross tolerance to other presynaptic inhibitory agents. 707 Feb 9

Long-term intake of ethanol decreases food intake and inhibits growth in experimental rats. The aim of this study was to determine the effect of 4-week oral ethanol ingestion on plasma leptin and adrenal function. Male 45-day-old Wistar rats were divided into three groups: absolute control (AC), ethanol (E) administered 10% (wt/vol) ethanol instead of tap water, and pair-fed (PF) given an amount of food corresponding to the food intake of E animals. E rats consumed less pelleted diet (74% cumulative total intake); however, this caloric deficit was compensated by ethanol ingestion. Net water intake in E animals was 76% of that in the control groups. The body growth of both E and PF rats was stunted compared with AC animals, but E rats were heavier than PF rats. The plasma leptin level was similar in E and AC and decreased in PF animals. There were no differences in plasma osmolality or glycemia among the three groups. Plasma insulin was decreased in PF compared with both AC and E rats. Plasma corticosterone was not affected by ethanol, but was increased in the food-restricted (PF) group. Although there were no differences in basal adrenal corticosterone production in vitro, there was a slightly higher response to corticotropin (ACTH) in E rats. We conclude that drinking 10% ethanol decreased the dietary intake and body growth. These changes were not mediated by plasma leptin changes. Although alcohol ingestion and its energy content theoretically normalized the total energy intake and prevented the decrease of plasma leptin, the growth of young rats was inhibited. Drinking 10% ethanol instead of tap water for 4 weeks did not stimulate basal adrenal activity.
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PMID:Four-week ethanol intake decreases food intake and body weight but does not affect plasma leptin, corticosterone, and insulin levels in pubertal rats. 978 33


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