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 anatomical and biochemical features of primary sensory afferents and the peptidergic innervation of cremaster motoneuron efferents in the genitofemoral (Gf) nerve were analyzed in the rat using immunohistochemical, histochemical, retrograde tracing and lesion methods. Afferent fibers in the Gf nerve were shown to originate from neurons in L1 and L2 dorsal root ganglia (DRG) and to project to L1 to T12.5 in the spinal cord. Some of the DRG neurons giving rise to these fibers contained substance P (SP) or the enzyme fluoride-resistant acid phosphatase but none appeared to contain somatostatin. The dermatome area of the Gf nerve, as determined by plasma extravasation methods, was located in the rostral scrotal and adjacent abdominal region. Identification of cremaster motoneurons by retrograde labelling from the Gf nerve revealed these neurons to be located in the L1 to L2 spinal cord segment, to have prominent rostrocaudally oriented dendritic aborizations and to receive a rich innervation by fibers containing SP, thyrotropin-releasing hormone (TRH) or met-enkephalin (met-Enk). Lesion studies indicated the SP-and met-Enk-containing fibers to be supplied by local intraspinal systems and the TRH-containing fibers by supraspinal systems. In female rats, motoneurons corresponding to the male version of the cremaster motoneuronal pool were less developed and received far fewer peptidergic connections than that observed in males. The multiple neural systems innervating cremaster motoneurons together with sensory afferents in the Gf and other scrotal nerves are suggested to be involved in the contribution of cremaster muscles to thermoregulation of the scrotum.
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PMID:Neural relations of cremaster motoneurons, spinal cord systems and the genitofemoral nerve in the rat. 393 95

A growing body of evidence suggests that neural peptides may induce important modulations on vegative and motor functions of the eye. The present study was designed to evaluate the effect of intracameral (I.C.) administration of alpha-melanocyte-stimulating hormone (alpha-MSH) and several other ocular peptides on intraocular pressure (IOP) in rabbits. alpha-MSH (5 micrograms) produced a significant and prolonged unilateral increase of IOP. This effect of I.C. alpha-MSH was dose-dependent (ED50 = 2.5 micrograms). Structure-activity studies revealed that equimolar doses of beta-MSH and gamma-MSH, unlike alpha-MSH, were totally ineffective. In addition, the structurally unrelated peptides beta-endorphin, thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (Gn-RH) did not affect IOP, when tested in a dose equimolar to 5 micrograms of alpha-MSH. These results confirm and extend previous observations, suggesting that alpha-MSH may be an important factor involved in regulation of IOP.
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PMID:Intracameral administration of alpha-MSH increases intraocular pressure in rabbits. 408 Jan 14

An assay for the binding of [(3)H]thyrotropin-releasing hormone ([(3)H]TRH) is described. Plasma membranes isolated from bovine anterior pituitary gland bind about 600 femtomoles of this hormone per mg of protein, as compared to 15 femtomoles per mg of protein in the total adenohypophyseal homogenate (40-fold purification). The equilibrium constant of membrane receptor-[(3)H]TRH binding at 0 degrees C is 4.3 x 10(7) L.M(-1), or a half-maximal binding of this hormone at 23 nM. The binding is time-dependent; addition of unlabeled hormone induces dissociation of the receptor-[(3)H]TRH complex with a half-life of 14 min. The binding of TRH is not altered by 10 muM melanocyte-stimulating hormone-release inhibiting hormone, lysine-vasopressin, adrenocorticotropin, growth hormone, prolactin, luteinizing hormone, insulin, glucagon, L-thyroxine, or L-triiodothyronine. K(+) and Mg(++) increase formation of the receptor-TRH complex at optimal concentrations of 5-25 mM and 0.5-2.5 mM, respectively, with inhibition at higher concentrations. Ca(++) inhibits binding of TRH at all concentrations tested.
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PMID:Binding of thyrotropin-releasing hormone to plasma membranes of bovine anterior pituitary gland (hormone receptor-adenylate cyclase-equilibrium constant-( 3 H)thyrotropin). 462 48

In a significant proportion of patients with acromegaly, a non-specific increase in plasma growth hormone (GH) has been recognized following administration of thyrotropin-releasing hormone (TRH) or luteinizing hormone-releasing hormone (LH-RH), probably due to the lack of the specificity of the receptor in their tumor cells. In this study, the effects of corticotropin-releasing factor (CRF), a newly isolated hypothalamic hormone, in addition to TRH and LH-RH, on plasma levels of GH and the other anterior pituitary hormones were evaluated in 6 patients with acromegaly. Synthetic ovine CRF (1.0 microgram/kg), TRH (500 micrograms) or LH-RH (100 micrograms) was given as an iv bolus injection, in the morning after an overnight fast. Blood specimens were taken before and after injection at intervals up to 120 min, and plasma GH, adrenocorticotropin (ACTH), thyrotropin, prolactin, luteinizing hormone, follicle-stimulating hormone and cortisol were assayed by radioimmunoassays. A non-specific rise in plasma GH was demonstrated following injection of TRH and LH-RH, in 5 of 6 and 2 of 5 patients, respectively. In all subjects, rapid rises were observed in both plasma ACTH (34.3 +/- 6.2 pg/ml at 0 min to 79.5 +/- 9.5 pg/ml at 30 min, mean +/- SEM) and cortisol level (9.1 +/- 1.3 micrograms/dl at 0 min to 23.4 +/- 1.2 micrograms/dl at 90 min). However, plasma levels of GH and the other anterior pituitary hormones did not change significantly after CRF injection. These results indicate that CRF specifically stimulates ACTH secretion and any non-specific response of GH to CRF appears to be an infrequent phenomenon in this disorder.
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PMID:Effect of synthetic ovine corticotropin-releasing factor on growth hormone secretion in patients with acromegaly. 609 67

Neurotensin (NT), administered intracisternally to mice, produced significant dose-dependent antinociception in three analgesic tests: tail immersion, hot-plate and acetic acid writhing. Naloxone (1-5 mg/kg), an opiate antagonist administered i.p. 20 min before NT administration, did not significantly alter NT-induced antinociception in any of these tests; naloxone did significantly reverse beta-endorphin-induced antinociception. However, centrally and peripherally administered thyrotropin-releasing hormone antagonized NT-induced (but not beta-endorphin-induced) antinociception. Equimolar doses of another tripeptide (Pro-Leu-Gly-NH2; melanostatin) did not alter the effects of NT. The data obtained in this study confirm NT-induced antinociception, provide further evidence that NT does not activate naloxone-sensitive opiate receptors and demonstrate that this brain effect of NT is antagonized by thyrotropin-releasing hormone. These findings therefore support the hypothesis that NT and thyrotropin-releasing hormone are functional antagonists in the central nervous system.
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PMID:Neurotensin-induced antinociception in mice: antagonism by thyrotropin-releasing hormone. 611 61

It has been previously demonstrated that thyrotropin-releasing hormone (TRH) stimulates in vitro the release of alpha-melanocyte-stimulating hormone (alpha-MSH) in frog. In the present study, the effects of various neuropeptides on spontaneous and/or TRH-induced alpha-MSH secretion were investigated, using a well-defined perifusion system technique. Vasoactive intestinal peptide, (VIP) a neurohormone which stimulates TRH target cells in mammals, was totally devoid of effect on frog melanotrophs although VIP-like material could be detected in neurointermediate lobe extracts. Somatostatin-like immunoreactive material was found in high concentrations in the frog neurointermediate lobe complex, but synthetic somatostatin (from 10(-10) to 10(-6) M) did not modify the spontaneous release of alpha-MSH. At doses of 10(-8) and 10(-6) M, synthetic somatostatin did not modify TRH-induced alpha-MSH secretion. Morphine (10(-5) M) and opioid peptides (10(-10) to 10(-6) M) had no effect on spontaneous alpha-MSH secretion. In addition, methionine enkephalin (10(-5) M) did not modify the stimulatory effect of TRH on alpha-MSH secretion. From these results we conclude that, among the neuropeptides which modulate prolactin secretion in mammals, only TRH is involved in alpha-MSH secretion in the frog.
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PMID:In vitro study of frog (Rana ridibunda Pallas) neurointermediate lobe secretion by use of a simplified perifusion system. III. Effect of neuropeptides on alpha-MSH secretion. 614 Feb 3

The source and topography of neuropeptide-containing axons in the median eminence are summarized. Several of these neuropeptide-containing neurons (thyrotropin-releasing hormone, corticotropin-releasing hormone, vasopressin, oxytocin, cholecystokinin) are localized in the paraventricular nucleus. The periventricular and medial preoptic nuclei constitute the main sources of somatostatin and luteinizing hormone releasing hormone axons in the median eminence, respectively. Dynorphins and alpha-neo-endorphin-synthetizing neurons in the supraoptic nucleus also project to the median eminence. Wherever they originate, the projections may follow a common organization pattern and use a common gate--the lateral retrochiasmatic area--to enter the median eminence.
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PMID:Neuropeptides in the hypothalamo-hypophyseal system: lateral retrochiasmatic area as a common gate for neuronal fibers towards the median eminence. 614 39

Because hypothalamic and extrahypothalamic levels of thyrotropin-releasing hormone immunoreactivity (TRH-IR) undergo profound changes during the prenatal and early postnatal period in rats, similar effects with advanced aging were anticipated. For this reason we measured hypothalamic and reproductive tissue levels of TRH-IR, hypothalamic levels of somatostatin (SRIF), and beta-endorphin (EP), serum levels of prolactin (Prl), growth hormone (GH), thyrotropin (TSH), and thyroxine (T4) in young, sexually mature and 24-28 month-old male Long-Evans and Sprague-Dawley rats. Hypothalamic and prostatic levels of TRH-IR were consistently reduced as were the levels of T4 in old rats compared to young controls. Aging did not change the ratio of TRH to the major TRH-like peptide in prostates, as determined by high pressure liquid chromatography (HPLC) or the levels of hypothalamic SRIF and EP. All of the hypothalamic TRH-IR in both old and young male rats consisted of TRH by HPLC. Falling hypothalamic TRH levels and TRH secretory capacity may play a role in the blunted TSH response to cold stress in old rats.
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PMID:Thyrotropin-releasing hormone levels decrease in hypothalamus of aging rats. 615 Nov 24

The effects of intracerebroventricular administration of several peptides on discrete-trial, conditioned avoidance responding were assessed in the rat. Three peptides (neurotensin, bombesin and beta-endorphin) produced a neuroleptic-like effect (i.e. a decrease in avoidance responding with no effect on escape responding). A low dose (0.6 nmol) of each peptide elicited a significant effect. Neurotensin and bombesin produced a significant but partial decrease in avoidance responding; larger doses of these peptides did not produce a greater effect. beta-Endorphin elicited dose-related decrements in avoidance responding. In addition, the effect of neurotensin, but not bombesin or beta-endorphin, was antagonized by simultaneous administration of an equimolar dose of thyrotropin-releasing hormone. Hence, the 3 peptides do not appear to produce decreases in avoidance responding by the same mechanism. Thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, bradykinin, substance P, des-Tyr1-gamma-endorphin and melanotropin inhibiting factor did not significantly affect avoidance responding. These findings, taken together with previous findings, suggest that intracerebroventricular administration of certain endogenous peptides (neurotensin, bombesin and beta-endorphin) may exert neuroleptic-like effects.
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PMID:The effects of neuropeptides on discrete-trial conditioned avoidance responding. 617 91

The switch from fetal to adult hemoglobin (Hb) has been investigated in fetal and newborn lambs. In the period between 125 and 145 days gestation, the proportion of fetal cells containing adult Hb increased significantly in catheterized fetuses. This increase paralleled the rise in fetal plasma cortisol under several different experimental conditions. However, infusion of synthetic adrenocorticotropin (ACTH1-24) into the fetus, which increased fetal plasma cortisol concentrations to levels slightly higher than observed at term, did not bring about any increase in the proportion of cells containing adult Hb. Increasing fetal plasma prolactin (PRL) concentration either by infusion of PRL or by stimulating endogenous PRL release with thyrotropin-releasing hormone (TRH) did not influence the time or rate of the switch. The fetal reticulocyte count was significantly higher in blood samples taken at the time of catheterization in fetuses of 103-115 days gestation than at 116-128 days gestation. In one repeatedly sampled fetus of adult type Hb AB, Hb C was observed at the time when the fetus was anemic. At birth the number of cells containing adult Hb was significantly higher in catheterized lambs than in nonoperated controls.
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PMID:Fetal and adult hemoglobin in the chronically catheterized sheep fetus. 618 97


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