Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The goal of this study was to examine the effects of melatonin, as well as those of melatonin and corticotropin (1-24 adrenocorticotrophic hormone (ACTH); Synacthen Depot) administered together, on the mitotic activity of adrenocortical cells in male and female mice. Melatonin was given subcutaneously once daily, in late-afternoon injections (between 16:00 and 18:00) in doses of 1 microgram, 10 micrograms, and 100 micrograms, and ACTH in a dose of 0.1 mg (10 U) daily for 10 days. Additionally, the highest dose of melatonin (100 micrograms daily) was administered together with ACTH. The metaphase-arrest technique using colchicine as a stathmokinetic agent was employed in the study. Melatonin, in all the examined doses, significantly decreased mean mitotic activity rate (MMAR) of the adrenal cortex in both male and female mice. Moreover, in a dose of 100 micrograms, melatonin suppressed the mitogenic effect of ACTH on the adrenal cortex. Furthermore, the present study investigated the effects of melatonin (5 x 10(-7)M), N-acetylserotonin (NAc-5HT) (5 x 10(-7)M), and ACTH (250 mU/ml or 1,000 mU/ml) alone as well as the effect of ACTH (250 mU/ml) applied jointly with melatonin on the mitotic activity of adrenocortical cells in rat adrenal explants incubated in vitro. Both pineal indoleamines (melatonin and NAc-5HT) significantly decreased the MMARs of adrenocortical cells. Corticotropin, as well as ACTH and melatonin applied together, also reduced the MMAR of adrenocortical cells. The present data suggest that melatonin may be directly involved in the inhibitory control of adrenocortical cell proliferation.
J Pineal Res 1989
PMID:Melatonin inhibits mitotic activity of adrenocortical cells in vivo and in organ culture. 272 51

This study examines the possible involvement of beta-endorphin in the photoperiodic control of reproduction in the Syrian hamster. beta-Endorphin and LHRH concentrations in the medial basal hypothalamus (MBH), anterior hypothalamus (AHA), and the preoptic area (POA) as well as pineal melatonin content were determined by RIA in male Syrian hamsters exposed to either a long day [(LD) 16-h light; 8-h dark; lights on 0700-2300] or short day [(SD) 8-h light, 16-h dark; lights on 0700-1500] for 8 weeks. Groups of eight animals from each photoperiod were killed by decapitation at 4-h intervals over 24 h. Twenty minutes before death half the animals from each photoperiod were given naloxone (5 mg/kg, sc), the other half saline. Exposure to a long photoperiod maintained testicular activity while a short photoperiod induced testicular regression. Pineal melatonin content in both photoperiods was maximal at 0500 h, i.e. 2 h before the onset of light (SD, 435.58 +/- 82.7 pg/pineal; LD, 276.78 +/- 56.8 pg/pineal). However, the duration of the nighttime rise in pineal melatonin content was increased in SD animals with elevated melatonin levels at 2100 h (157.10 +/- 41.8 pg/pineal) and 0100 h (199.11 +/- 58.9 pg/pineal). In contrast pineal melatonin content in LD animals was only higher than daytime values at 0500 h. A daily rhythm of beta-endorphin content within both the AHA and MBH of animals exposed to a short photoperiod coincided with this prolonged nighttime rise in pineal melatonin content, although a causal relationship between the two was not established. Peak levels of beta-endorphin occurred at 2100 h (AHA, 6.569 +/- 1.2 pmol/mg protein; MBH, 4.877 +/- 0.45 pmol/mg protein) and at 0100 h (AHA, 6.107 +/- 0.66 pmol/mg protein; MBH, 4.49 +/- 00.79 pmol/mg protein) which was 6 h and 10 h into the dark phase, respectively, with lowest levels in the middle of the light phase (AHA, 3.561 +/- 0.56 pmol/mg protein; MBH, 2.688 +/- 0.3 pmol/mg protein). This rhythm was absent in animals exposed to a long photoperiod. There was no effect of photoperiod or time of day on the content of beta-endorphin in the POA. LHRH levels were not altered by changes in photoperiod in all three brain regions studied. In the AHA and MBH, concentrations of LHRH were similar at all times of day whereas, in the POA, LHRH levels varied with time in both photoperiods. Peak levels occurred in the middle of the dark phase at 0100 h (LD, 2.774 +/- 0.24 pmol LHRH/mg protein; SD, 3.206 +/- 0.48 pmol LHRH/mg protein) with lowest levels during the light phase (LD, 1.664 pmol LHRH/mg protein; SD, 1.775 pmol LHRH/mg protein).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in photoperiod alter the daily rhythms of pineal melatonin content and hypothalamic beta-endorphin content and the luteinizing hormone response to naloxone in the male Syrian hamster. 315 63

Adult female golden hamsters were used to study the effect of short photoperiod on the endogenous opioid system and the effect of pinealectomy on the serum beta-endorphin-like immunoreactivity (beta-end LI) levels. Hamsters were housed under either long photoperiod (14L:10D) or short photoperiod (2L:22D) and the regularity of the estrous cycles was determined by daily vaginal exfoliative cytology. Hamsters under short photoperiod became acyclic after about 7 wk. At the end of 8 wk, all the hamsters were decapitated and medial basal hypothalamic (MBH) content of LHRH and methionine-enkephalin (met-enkephalin) were measured by specific radioimmunoassays (RIA). Both LHRH and met-enkephalin levels of the MBH were significantly elevated in the short-photoperiod hamsters as compared to the normally cycling control animals under long photoperiod. In a second experiment, the effect of pinealectomy (PNX) on the serum levels of beta-end LI in the short-photoperiod hamsters was determined. The serum beta-end LI levels were increased approximately threefold in the noncyclic hamsters housed under 8 wk of short-photoperiod conditions. Pinealectomized hamsters kept under 8 wk of short-photoperiod exhibited lower serum beta-end LI levels similar to those of normally cycling hamsters kept under long photoperiod. These results indicate a possible functional relationship between increased pineal activity (as a result of short photoperiod) and increased MBH met-enkephalin, LHRH, and serum beta-end LI levels.
J Pineal Res 1984
PMID:Effect of short photoperiod on hypothalamic methionine-enkephalin and LHRH content and serum beta-endorphin-like immunoreactivity (beta-end LI) levels in golden hamsters. 610 Jul 20

Lewis (LEW/N) and Fischer (F344/N) rats are histocompatible inbred strains characterized, respectively, by susceptibility and resistance to inflammatory disease. The susceptibility of LEW/N rats to inflammation has been associated with deficient corticotropin-releasing hormone (CRH), ACTH, and corticosterone responses to inflammatory stimuli, specifically attributed to a global impairment in hypothalamic CRH neuron function. In contrast to the LEW/N rats, F344/N rats demonstrate an intact hypothalamic-pituitary-adrenal (HPA) axis. Melatonin, a neurohormone initially isolated in the pineal gland, has been implicated with inhibition of the HPA axis. To investigate melatonin synthesis and secretion in LEW/N and F344/N rats, we examined the diurnal activity of pineal arylalkylamine N-acetyltransferase (NAT1), the rate-limiting enzyme in melatonin biosynthesis, which demonstrates circadian rhythmicity, as well as the diurnal levels of serum melatonin, in both strains. Arylamine N-acetyltransferase (NAT2), a related enzyme activity, thought not to be regulated in a circadian manner, was examined as a control of NAT1 activity. Pineal NAT1 activity peak was observed later and reached significantly higher levels in LEW/N than in F344/N rats. Serum melatonin levels reflected the circadian pattern of the NAT1 activity, without, however, showing any quantitative differences between the two strains. Time-course of pineal NAT1 activity response to beta-adrenergic stimulation was parallel in the two rat strains, whereas the magnitude of the response as greater in LEW/N than in F344/N rats. No circadian or major quantitative differences in NAT2 activity were found between the two strains. Size-exclusion HPLC chromatograms of NAT1 activity revealed similar patterns in both rat strains.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differences in arylalkylamine N-acetyltransferase activity between inflammatory disease-susceptible Lewis and -resistant Fischer rats. 756 41

Some physiological parameters of pineal 5 alpha-dihydrotestosterone receptor in the rat such as ontogeny, circadian rhythm pattern, and its modulation by various neuropeptides and neurotransmitters which have profound influences on the pineal hormone melatonin were examined. Pineal 5 alpha-dihydrotestosterone receptors measured at different ages of the animal revealed that on day 10 both cytosolic receptor (CR) and nuclear receptor (NR) levels were high. With growth and development both groups of receptors declined and during puberty started again to rise. During adulthood both receptors were high; however, NR rose further with full maturation. Both groups of receptors showed circadian rhythmicity. While the CR was significantly higher at 6.00 h than at any time point through 24 h, the NR peaked at 18.00 h when the difference between both groups was maximum. Castration caused significant increment of NR. Treatment of castrated animals with a low dose of testosterone propionate (0.25 mg) significantly stimulated both receptor groups, while treatment with a high dose (2.5 mg) failed to do so. Treatment with various substances such as antiandrogen, opioids, neuropeptides, and neurotransmitters significantly modulated the pineal androgen receptor population: cyproterone acetate and monosodium glutamate suppressed CR; growth hormone releasing hormone increased NR; growth hormone release inhibiting hormone had no significant effects on either group of receptors; exogenous melatonin and norepinephrine increased NR; beta-endorphin increased only NR, but methionine enkephalin stimulated both, and epithalamine had no significant effects on either group of receptors, but thymosin alpha 1 increased NR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ontogeny, circadian rhythm pattern, and hormonal modulation of 5 alpha-dihydrotestosterone receptors in the rat pineal. 809 77

The effect of intracerebroventricular (i.c.v.) injection of melatonin and/or beta-endorphin on the [3H]flunitrazepam binding sites in the cerebral cortex of pinealectomized or superior cervical ganglionectomized rats was studied. Pinealectomy decreased the maximum concentration of benzodiazepine receptors (Bmax) without affecting the dissociation constant (KD), while melatonin, ineffective in control animals, counteracted the effect of pinealectomy. Intracerebroventricular injection of beta-endorphin increases Bmax in both control and pinealectomized animals, the effect being significantly higher in the latter. Simultaneous i.c.v. injection of melatonin + beta-endorphin did not further increase Bmax in any group, whereas i.c.v. injection of naloxone significantly blocked the effects of melatonin and/or beta-endorphin administration. Pineal sympathetic denervation produced a significant increase in Bmax and KD, whereas i.c.v. injection of melatonin further increased the former, restoring KD to control values. Neither i.c.v. administration of beta-endorphin or melatonin + beta-endorphin significantly modified the ganglionectomy-dependent increase in Bmax, although both treatments restored KD to control values. Naloxone administration had no effect on beta-endorphin- and melatonin + beta-endorphin-treated ganglionectomized groups, but counteracted the increased effect of melatonin on Bmax in ganglionectomized animals.
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PMID:Melatonin counteracts pinealectomy-dependent decreases in rat brain [3H]flunitrazepam binding through an opioid mechanism. 815 91

To obtain information on long-term circadian consequences of administering melatonin neonatally to rats, we assessed the 24-hour rhythms of 1) serum prolactin (PRL), luteinizing hormone (LH), and growth hormone (GH), and 2) medial basal hypothalamic dopamine (DA) and serotonin (5-HT) metabolism and corticotropin-releasing hormone (CRH) content in 60-day old male rats injected with 100 micrograms of melatonin on the 5th day of life. Controls receiving vehicle alone showed serum PRL concentration (when 60 days of age) attaining its maximum at the end of the light period (i.e., at 2000 hr), while in melatonin-injected rats high PRL values were found between 1200 and 2000 hr. Twenty-four hour changes in serum LH levels exhibited a maximum at noon, and to a similar extent in vehicle- and melatonin-treated rats. Neonatal melatonin injection did not affect serum GH concentration when the rats were adult. In the medial basal hypothalamus (MBH), the dihydroxyphenyl acetic acid (DOPAC)/ DA ratio attained a maximum at midnight, its amplitude being significantly higher in melatonin- than in vehicle-treated rats. Neonatally melatonin-injected rats also exhibited a second maximum in DOPAC/DA ratio at noon, coinciding with a minimum in DA levels of MBH. The 5-hydroxyindoleacetic acid (5-HIAA)/5-HT ratio in MBH showed significant diurnal variations in vehicle-injected controls with maxima at 1200 and 0400 hr, while in melatonin-treated rats a single maximum occurred at 2400 hr. These maximum correlated with minima in 5-HT content of MBH. Neonatal melatonin injection brought about a significant increase in the CRH content of MBH, as well as distortion of its diurnal rhythmicity, a maximum being found at noon in controls and at 1800 hr in melatonin-treated rats. The results indicate that exposure to melatonin early in life affects subsequent diurnal rhythmicity of PRL release, and of DA and 5-HT turnover and CRH content in the MBH of rats.
J Pineal Res 1997 Jan
PMID:Twenty-four hour rhythms of serum prolactin, growth hormone and luteinizing hormone levels, and of medial basal hypothalamic corticotropin-releasing hormone levels and dopamine and serotonin metabolism in rats neonatally administered melatonin. 906 71

An interaction between melatonin and adrenocorticotropin (ACTH) seems to occur in humans and both hormones respond to beta-adrenergic stimulation. As in lower animal species, human pineal gland also contains alpha2-adrenergic receptors as does the hypothalamus-pituitary axis. In this study the response of the pineal gland and of the hypothalamus-pituitary-adrenal axis to alpha2-adrenergic stimulation was assessed. Twenty-nine children (21 males, mean age 11.2 +/- 0.6 yr and eight females, mean age 9.1 +/- 1.1 yr) from the University of Granada Hospital were studied. The children were diagnosed as having growth problems but with a normal response of growth hormone (GH) to clonidine test. Changes in plasma levels of ACTH, cortisol and melatonin were evaluated in these children after oral administration of the alpha2-adrenoceptor agonist clonidine (100 microg/m2) or a placebo. Plasma ACTH, cortisol and melatonin were measured before (basal) and at 30, 60 and 90 min after oral clonidine or placebo administration. Hormonal determinations were carried out by commercial radioimmunoassay kits, previously standardised in our laboratory. The results show a significant decrease in plasma ACTH, cortisol and melatonin 30 min after clonidine administration (P < 0.001), reaching lowest values at 90 min after the drug was administered. The reduction in the levels of these hormones is independent of their normal circadian decay since the control group showed a significantly different pattern of behaviour. These data support the existence of an inhibitory alpha2-adrenergic influence on both the pineal gland and the hypothalamus-pituitary-adrenal in children and further support the presence of alpha2-adrenoceptors in the human pineal gland.
J Pineal Res 2000 Aug
PMID:Effect of clonidine on plasma ACTH, cortisol and melatonin in children. 1094 40

Both plasma melatonin levels and hypothalamic arcuate nucleus pro-opiomelanocortin (POMC) (biosynthetic precursor to the endogenous opioid ss-endorphin and other opiomelanocortins) mRNA content decrease with aging. To test whether the decline in melatonin is responsible for the decline in POMC mRNA, we investigated the effects of daily melatonin treatment on hypothalamic POMC mRNA content in middle-aged and older Sprague-Dawley rats. Daily nocturnal melatonin treatment (50 microg kg bw(-1) night(-1), in the night-time drinking water) for 7 months, starting at 13 months of age, did not significantly alter female arcuate nucleus POMC mRNA content determined at the end of the light period (i.e., before nightly melatonin administration), but suppressed (24%, P < 0.05) POMC mRNA content at the end of the dark period (i.e., following melatonin administration). Likewise, nocturnal administration of 50 or 500 microg melatonin kg bw(-1) night(-1) to male rats for 7 months suppressed (31 or 28%, respectively; P < 0.05) POMC mRNA content at the middle of the dark period at 20 months of age. Finally, 10 wk administration of 30 microg melatonin kg bw(-1) day(-1) suppressed (31%, P < 0.01) POMC mRNA content in middle-aged male rats killed at the end of the dark period. Melatonin treatments did not significantly alter estradiol or testosterone levels. Thus, moderate-dosage nocturnal melatonin supplementation suppressed nocturnal hypothalamic POMC gene expression in both middle-aged males and females, suggesting that melatonin supplementation during aging decreases, rather than increases, forebrain opiomelanocortinergic activity. These POMC responses were apparently not dependent on gonadal steroid responses and did not become refractory to melatonin treatment maintained until old age.
J Pineal Res 2003 Mar
PMID:Suppression of hypothalamic pro-opiomelanocortin (POMC) gene expression by daily melatonin supplementation in aging rats. 1256 4

Atopic dermatitis (AD), also known as atopic eczema, is chronic pruritic skin disease. AD can increase psychological stress as well, increasing glucocorticoid release and exacerbating the associated symptoms. Chronic glucocorticoid elevation disturbs neuroendocrine signaling and can induce neuroinflammation, neurotoxicity, and cognitive impairment; however, it is unclear whether AD-related psychological stress elevates glucocorticoids enough to cause neuronal damage. Therefore, we assessed the effects of AD-induced stress in a mouse AD model. AD-related psychological stress increased astroglial and microglial activation, neuroinflammatory cytokine expression, and markers of neuronal loss. Notably, melatonin administration inhibited the development of skin lesions, scratching behavior, and serum IgE levels in the model mice, and additionally caused a significant reduction in corticotropin-releasing hormone responsiveness, and a significant reduction in neuronal damage. Finally, we produced similar results in a corticosterone-induced AD-like skin model. This is the first study to demonstrate that AD-related psychological stress increases neuroendocrine dysfunction, exacerbates neuroinflammation, and potentially accelerates other neurodegenerative disease states.
J Pineal Res 2017 Sep
PMID:Melatonin inhibits neuronal dysfunction-associated with neuroinflammation by atopic psychological stress in NC/Nga atopic-like mouse models. 2850 Jul 66


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