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 effects of neonatal exposure to delta-9-tetrahydrocannabinol (THC) on the adult animal brain neurochemistry and pain perception were evaluated. Newborn rat pups were culled to a litter size of 8 (males and females) and treated either with THC (2 mg/kg) or oil (control) daily, during days 1-4 after birth. After weaning, the THC-treated males were housed 4 per cage. During the juvenile period (day 50), the THC-treated animals exhibited significantly lower baseline tail-flick values (a measure of pain perception) than the control. However, as adults, the THC-treated animals exhibited significantly higher sensitivity to pain following 5 mg/kg morphine challenge. Furthermore, the THC-treated animals had significantly elevated beta-endorphin and methionine-enkephalin levels in almost all the brain areas sampled for the study. In addition, the neonatally THC-treated rats exhibited significantly higher levels of substance P (SP) and significantly lower levels of gonadotropin releasing hormone (GnRH) in the anterior hypothalamus-preoptic area. The SP and GnRH levels did not differ among the THC-treated and control animals in the medial basal hypothalamus. The results of this study indicate that even a very low dose of THC administered during the neonatal period has a long-lasting effect on the brain neurochemistry. In particular, neonatal administration of THC appears to alter functioning of the endogenous opioid system.
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PMID:Effect of early exposure to delta-9-tetrahydrocannabinol on the levels of opioid peptides, gonadotropin-releasing hormone and substance P in the adult male rat brain. 170 Sep 26

The outer cortex of the human thymus contains a one- to two-cell-thick layer that is immunoreactive with antisera against beta-endorphin, (Leu)- and (Met)-enkephalin, bombesin, and substance P. The epithelial nature of these immunostained cells is revealed by immunoelectron microscopic studies showing the presence of desmosomal junctions. The presence of peptide-containing cells in the outer cortex, where the most immature and recently immigrated thymocytes are found, emphasizes the role of neuropeptides in regulating the microenvironment for T cell development.
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PMID:Neuropeptide-immunoreactive cells in human thymus. 170 21

The effects of single and repeated doses of met-enkephalin (Met-E) on the ultrastructure and TSH-like immunoreactivity (IR) of pituitary TSH-producing cells, and TSH plasma levels in male rats and the influence of pretreatment with a dopamine antagonist, haloperidol, on these, were evaluated. Both acute and repeated Met-E administration produced changes in TSH cells consisting of: an increase in TSH-like IR, enlargement and dilation of RER and Golgi apparatus, size-increase of secretory granules, and the presence of a variable number of cytoplasmic vacuoles. The ultrastructural changes were more evident in the chronically treated animals, whereas no differences were found in IR-intensity between both Met-E treated groups. Haloperidol alone modifies neither ultrastructure nor TSH-like IR of TSH producing cells, but it prevented the Met-E produced changes. On the other hand, Met-E treatment resulted in a decrease of TSH plasma levels, but being significant only in the acutely injected animals. No variations were produced by haloperidol alone, but it prevented the decrease of TSH plasma levels stimulated by Met-E. Our results suggest that Met-E plays a role in the release of TSH, and that dopamine is implicated in this process. The possible mechanisms through which Met-E influences TSH secretion are discussed.
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PMID:Study of the rat TSH-producing cells after met-enkephalin treatment: effects of dopamine antagonists. 176 27

The substrate specificity of polysome rat liver N alpha-acetyltransferase (NAT) has been examined by utilizing a series of synthetic and natural substrates that has been systematically altered with respect to N-terminal sequence and length. Families of peptides of the structure S-Y-S-G-G-L-L-L were generated by successively replacing the N-terminal serine, the penultimate tyrosine, and the antepenultimate serine with all 19 commonly occurring amino acids, which were then assessed for their reactivity with the rat liver enzyme. Only peptides with N-terminal serine, alanine, methionine, leucine, and phenylalanine were modified. Glycine, lysine, arginine, valine, isoleucine, and tryptophan in the second position are (with N-terminal serine) strongly inhibitory, and proline completely blocks modification. Third-position substitutions have less of an effect on NAT activity with glycine, aspartic acid, glutamic acid, and tryptophan being most inhibiting (with N-terminal Ser-Tyr). These observations are generally in agreement with in situ modifications although there are some significant differences particularly with respect to the amino-terminal residues. Optimal chain length was determined to be 10-11 residues with either synthetic peptides of the structure S-Y-S-(G)n-L-L-L or adrenocorticotropin (ACTH) sequences ranging from 8 to 39 residues. The ACTH peptides were generally found to be severalfold better substrates than the corresponding synthetic ones. Activity was not affected by increased chain length beyond approximately 17 residues. These data support the view that polysome-catalyzed N alpha-acetylation occurs as a cotranslational event on nascent chains of about 20-40 amino acids in length.
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PMID:Rat liver polysome N alpha-acetyltransferase: substrate specificity. 184 56

Plasma met-enkephalin immunoreactivity (MET-ENKi) and catecholamine levels were measured in umbilibal cord blood from 46 healthy newborn infants. Clinical data including Apgar scores, birth weight, gestational age, route of delivery, fetal heart tracings and arterial blood gas values were also obtained. Thirty-nine infants were delivered by the vaginal route. All but 1 infant delivered by cesarian section had undergone a trial of labor. Plasma MET-ENKi in the newborn infants was markedly greater than levels found in healthy adult volunteers: 360 +/- 25 versus 25 +/- 2 pg/ml, respectively. MET-ENKi levels were similar in umbilical arterial and umbilical venous blood, and in infants delivered vaginally or by cesarian section.
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PMID:Plasma methionine enkephalin levels in the human newborn at birth. 193 84

The effect of morphine tolerance-dependence, protracted and naloxone-precipitated abstinence on the levels of beta-endorphin and methionine-enkephalin in discrete brain regions, spinal cord, pituitary gland and plasma was determined in the male Sprague-Dawley rats. Among the brain regions examined, the levels of beta-endorphin in descending order were: hypothalamus, amygdala, midbrain, hippocampus corpus striatum, pons and medulla and cortex. The levels of beta-endorphin in midbrain, hypothalamus, and pituitary of morphine tolerant-dependent rats were decreased significantly. During protracted withdrawal beta-endorphin levels were decreased in amygdala, spinal cord and pituitary. During naloxone-precipitated abstinence beta-endorphin levels were increased in corpus striatum, midbrain and cortex. In addition, in naloxone-precipitated abstinence beta-endorphin levels were decreased in pituitary gland and hippocampus but increased in plasma. The levels of methionine-enkephalin in brain regions in decreasing order were: corpus striatum, pons and medulla, amygdala, hypothalamus, midbrain, hippocampus and cortex. The levels of methionine-enkephalin in pons and medulla, amygdala, hippocampus and pituitary gland were decreased in morphine tolerant-dependent rats. During protracted abstinence from morphine, methionine-enkephalin levels in spinal cord, amygdala, pons and medulla, midbrain, cortex, corpus striatum and pituitary gland were decreased. The levels of methionine-enkephalin in hypothalamus and corpus striatum of naloxone-precipitated abstinent rats were increased but were decreased in amygdala and pituitary gland. These results suggest that during morphine tolerance-dependence and during protracted abstinence beta-endorphin and methionine-enkephalin levels in discrete brain regions and pituitary gland are decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin and methionine-enkephalin levels in discrete brain regions, spinal cord, pituitary gland and plasma of morphine tolerant-dependent and abstinent rats. 193 85

Evidence for the presence of an enkephalinergic system in the ganglia of the pond snail, Lymnaea stagnalis, has been obtained with 3 experimental approaches. Scatchard analysis with [3H]etorphine reveals a monophasic high-affinity opiate binding site (Kd 2.3 nM) which is naloxone-sensitive. Immunocytochemical localization of Met- and Leu-enkephalin-like substances as well as alpha-MSH- and ACTH-like materials was demonstrated within specific populations of neurons. Substances with Met- and Leu-enkephalin and Met-enkephalin sulfoxide RIA reactivities were detected also in HPLC fractions corresponding to the retention times of authentic enkephalin standards. Together, the results provide strong evidence for the presence of enkephalinergic mechanisms in the nervous system of Lymnaea stagnalis. Additionally, the report provides indirect evidence for the existence of a macromolecular opioid precursor. This enkephalinergic system shows striking similarities to opioid mechanisms found in vertebrates and bespeaks a common evolutionary origin.
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PMID:Evidence for an enkephalinergic system in the nervous system of the pond snail, Lymnaea stagnalis. 196 5

Precursors to beta-endorphin (BE) and methionine enkephalin (ME), and proteolytic enzymes that cleave those BE and ME precursors to BE and ME, were determined in several milliliters of human cerebrospinal fluid. Endogenous peptides were purified by reversed-phase high-performance liquid chromatography (HPLC), and were detected with radioreceptor assay (RRA), radioimmunoassay, and mass spectrometry (MS). Total opioid receptor activity measurements and the profile of HPLC-receptor activity of human CSF samples were both used to monitor neuropeptide metabolism. MS data linked the molecular ion of ME to a unique fragment ion. A later-eluting fraction (84 min) in a 90-min HPLC gradient appeared in all HPLC-RRA profiles, contained opioid receptor activity that displaced [3H]etorphine, and the quantitative and qualitative patterns of opioid receptor activity in those profiles both changed within the few minutes that elapsed between acquiring the first and second cerebrospinal fluid samples. That 84-min fraction contained precursors to opioid peptides and was fractionated further with a more shallow 120-min HPLC gradient into three sections that displayed delta-opioid receptor-preferring activity, using [3H]ME as ligand. These three sections were hydrolyzed separately with human cerebrospinal fluid as the source for endogenous neuropeptides to yield products that correlated to immunoreactive BE in section I and immunoreactive ME in section III.
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PMID:Proenkephalin A and proopiomelanocortin peptides in human cerebrospinal fluid. 196 61

Effects of the glucocorticoid milieu on the basal and ether stress-induced prolactin (PRL) release and on the immunostaining for hypothalamic vasoactive intestinal peptide (VIP), beta-endorphin (beta-EP), dynorphin-A (DYN-A) and methionine-enkephalin (Met-ENK), were examined in separate groups of male rats. After colchicine treatment in intact rats, VIP-containing cell bodies were observed only in the suprachiasmatic nucleus (SCN). Adrenalectomy (ADX), performed 7 days previously, resulted in the additional appearance of VIP-immunoreactive neurons in the parvocellular subdivision of the paraventricular nucleus (PVN), as well as in significantly higher basal and stressed PRL levels than intact values. Treatment of intact rats with a high dose (500 micrograms/kg body weight (s.c.) daily for 7 days) of dexamethasone (DEX), but not with a low dose (50 micrograms/kg) of DEX, significantly reduced both the basal and stressed PRL release. Administration of either the low or high dose of DEX to ADX rats prevented the appearance of the PVN-VIP neurons. In addition, the ADX-induced high basal and stressed PRL levels were restored to intact values by the low dose of DEX, and completely suppressed by the high dose of DEX. The staining of SCN-VIP-, beta-EP-, DYN-A or Met-ENK neurons was not affected by any treatment employed in this study. These results suggest that the appearance of PVN-VIP immunostaining in ADX rats may, at least in part, be responsible for the enhanced PRL secretion observed in this group. However, SCN-VIP-, beta-EP-, DYN-A- or Met-ENK neurons do not seem to play a pivotal role in the glucocorticoid regulation of PRL secretion.
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PMID:The immunostaining for the hypothalamic vasoactive intestinal peptide, but not for beta-endorphin, dynorphin-A or methionine-enkephalin, is affected by the glucocorticoid milieu in the rat: correlation with the prolactin secretion. 197 81

The influences of opioids on pial arteriolar diameter and cortical periarachnoid cerebrospinal fluid prostanoid concentration were investigated in piglets with closed cranial windows. Methionine enkephalin (10(-12)-10(-6) M) increased pial arteriolar diameter (139 +/- 4, 149 +/- 3, 178 +/- 3 microns, for control, 10(-12), and 10(-6) M, respectively). Leucine enkephalin produced similar pial arteriolar dilation. In contrast, dynorphin elicited dilation during normotension and constriction during hypotension. beta-Endorphin (10(-12)-10(-6) M) decreased pial arteriolar diameter (137 +/- 6, 128 +/- 6, 92 +/- 7 microns, for control, 10(-12) and 10(-6) M, respectively). All four opioids increased cerebrospinal fluid 6-keto-prostaglandin (PG)F1 alpha, PGE2, PGF2 alpha and thromboxane B2. Indomethacin (5 mg/kg i.v.) blocked methionine and leucine enkephalin and dynorphin-induced pial arteriolar dilation, but potentiated beta-endorphin-induced constriction and the constriction caused by dynorphin in hypotensive piglets. These data indicate that prostanoids modulate opioid effects on the cerebral vasculature.
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PMID:Prostanoids modulate opioid cerebrovascular responses in newborn pigs. 197 12


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