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

Both direct pituitary and indirect CNS mechanisms have been postulated for the influence of opiate agonists on prolactin secretion. By examining the interactions between terminals of neurons containing opioid peptides and hypothalamic TH-positive cell bodies, this paper addressed the anatomical basis for the latter mechanism. Initial electron microscopic studies directly demonstrated contact between opioid peptide terminals and dopaminergic cell bodies and provided some visual criteria for assessing opioid-dopamine interactions at the light microscopic level. Using these guidelines, we examined the rates of contact on both A12 and A14 neurons of each of the three opioid peptide families: pro-enkephalin, pro-dynorphin, and pro-opiomelanocortin (POMC). For A14 neurons, many of which project to the posterior pituitary, contact rates were estimated at 15, 20, and 5% for dynorphin, Met-enkephalin, and ACTH (a POMC derivative), respectively. In contrast, the A12 dopamine neurons, which regulate prolactin secretion by inhibition, showed a roughly 70% contact rate with dynorphin axons (P less than 0.001) with Met-enkephalin and ACTH contact rates remaining low at 20 and 5% respectively. Contact frequency varied significantly during the estrus cycle only with dynorphin contacts on A12 neurons. Proestrus and diestrus (less so) showed a small but significant (P less than 0.05) elevation in contact rates versus estrus, male, lactating and pregnant groups. No other significant difference emerged among these groups. On the basis of these observations, we conclude that dynorphin represents a significant and specific factor in the innervation of A12 dopamine neurons. This relationship may account for some if not most of the influence of opiate agonists and antagonists on prolactin secretion.
 ...
PMID:Interaction of opioid peptide-containing terminals with dopaminergic perikarya in the rat hypothalamus. 149 60

Enkephalin and morphine initiation of phase III of MMC has been reported in dog and humans. In chickens, a similar migrating activity initiated at the duodenum occurs 7-9 times a day while the gastric activity ceases. The main objective was to determine whether this migrating activity could be induced by opioids. Electrodes for electromyography were implanted in the stomach, proximal and distal duodenum, jejunum and proximal and distal ileum of 4 wk old chickens. Met-enkephalin, morphine and beta-casomorphin-5 (5 x 10(-7) moles/Kg) were infused i.v.. All these substances initiated an intestinal migrating activity concurrent with gastric inhibition. The mean duration of gastric inhibition depended on the substance, lasting from 5 min (met-enkephalin) to 27 min (beta-casomorphin-5). The migrating activity started in the distal duodenum and propagated to the ileum in about 18 min. These effects were partially blocked by naloxone at equimolar doses. In conclusion, in chickens, as in dogs and humans, migrating myoelectrical activity can be initiated by opioids.
 ...
PMID:Opioid-induction of migrating motor activity in chickens. 154 51

In a double-blind crossover study of 10 normal healthy subjects, we examined the effects of slow-release nifedipine (nifedipine-SR, 10 mg b.i.d) administration on exercise capacity, hormone levels during exercise, and quality of life (QOL) after a 2-week treatment. Two exercise tests, a progressive exercise test and a constant work-rate exercise test, were performed. Maximal oxygen uptake (VO2max) and blood lactate concentration were measured during the progressive exercise test and the exercise intensity corresponding to half lactate threshold (LT), LT, and 4 mmol/l of lactate concentration was determined. Subjects underwent 20 minutes of constant work-rate exercise at each work load, and blood lactate, plasma epinephrine, plasma norepinephrine, plasma renin activity, plasma aldosterone, atrial natriuretic peptide, plasma beta-endorphin, and met-enkephalin were measured. Taking nifedipine-SR had no effect on the responses of blood pressure, heart rate, VO2max, maximal work load, and LT compared to taking placebo. Blood lactate, plasma catecholamine, plasma renin activity, aldosterone, atrial natriuretic peptide, and beta-endorphin levels increased during exercise, and there was no difference between nifedipine-SR and placebo. Met-enkephalin did not increase with either treatment. In the QOL questionnaires, no differences were noted between the two treatments. These findings suggest nifedipine-SR to be a potentially useful drug in view of the lack of effect on exercise capacity, hormone release, and QOL.
 ...
PMID:Administration of slow-release nifedipine does not affect lactate threshold, hormone release during exercise, and quality of life in normal subjects. 157 99

The present study compared the effects of partial sleep deprivation and the effects of an intake of a hypnotic compound (zolpidem) prior to bedtime, on sleep and on hormonal and metabolic adaptations to subsequent exercise. Sleep deprivation consisted of a delayed bedtime and an early getting-up time. Eight young subjects, who slept well and were highly trained athletes, were enrolled in this study. Sleep was recorded polygraphically and the following afternoon exercise was performed on a cycle ergometer for 30 min at 75% of maximal oxygen consumption (VO2max) after a 10-min warm up. Met-enkephalin, beta-endorphin, cortisol, and lactate concentrations were measured at rest and during exercise. The data obtained after experimental sleep, with and without medication were compared with those obtained in the reference condition with normal sleep. Both types of sleep reduction decreased the total sleep time, stage 2 sleep, and rapid eye movement sleep, whereas zolpidem administration did not modify either the duration of sleep or the sleep stages. After the reference night, plasma met-enkephalin did not show any significant change at the end of the submaximal exercise, whereas beta-endorphin, cortisol, and lactic acid concentrations increased significantly in all subjects. The changes in concentration in beta-endorphin were significantly related to the changes in cortisol (r = 0.78; P less than 0.01) and to the changes in plasma lactic acid (r = 0.58; P less than 0.05). Cortisol concentrations were also related to lactic acid values (r = 0.94; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Met-enkephalin, beta-endorphin and cortisol responses to sub-maximal exercise after sleep disturbances. 159 64

The neurotoxic effects produced by ibotenic acid (IA) induced chemical lesions of the central nervous system (CNS) cholinergic system were examined on the opioid peptidergic system in adult rats. Forebrain cholinergic systems were bilaterally lesioned by the infusion of IA (1 or 5 micrograms/site) into the nucleus basalis magnocellularis (NBM). One week after the injections, the animals were sacrificed, and activities of acetylcholinesterase (AChE), choline acetyltransferase (ChAT) and concentrations of beta-endorphin (beta-End) and Met-enkephalin (Met-Enk) were measured in different brain regions. Animals treated with IA showed a decrease in the activity of ChAT (-24%), AChE (-36%) and beta-End level (-33%) in the frontoparietal cortex (FC). For the first time we report that these changes were associated with a compensatory increase in the activity of ChAT (+27%), AChE (+25%), beta-End level (+66%) in the remaining part of the cortex, i.e. cortex devoid of frontal cortex (C-FC). Met-enkephalin level increased by 59% in the frontoparietal cortex and did not change in the cortex devoid of frontal cortex upon IA treatment. These results suggest that IA treatment results in changes in the activity of cortical ChAT and AChE, and beta-End level in the same direction. Injection of IA in the NBM did not cause a change in the activity of ChAT or AChE in other brain regions such as hippocampus, striatum or midbrain. In addition to cortex devoid of frontal cortex, midbrain also showed a significant increase in the beta-End level in the IA treated animals. However, pituitary beta-End decreased in the neurotoxin treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The neurotoxic actions of ibotenic acid on cholinergic and opioid peptidergic systems in the central nervous system of the rat. 161

The level of opioid peptides in several brain areas and in the pituitary was estimated in WAG/Rij rats, which are considered to be a genetic animal model for human absence epilepsy. In comparison with three groups of non-epileptic controls, these epileptic rats had an elevated level of the proenkephalin-derived peptide Met-enkephalin-Arg6-Gly7-Leu8 in the mesencephalon and striatum, while the level of the prodynorphin-derived peptide alpha-neoendorphin was increased in the striatum and hippocampus. In addition various age- and/or strain-related changes in these peptide levels were found in the hippocampus, thalamus, striatum, frontal cortex and neurointermediate lobe of the pituitary. No difference in the hypothalamic beta-endorphin level were found between epileptic and non-epileptic rats, though strain- and/or age-related changes in the peptide content were detected in both lobes of the pituitary. The increased level of proenkephalin and prodynorphin opioid peptides in brain structures, essential for the appearance of spike-wave discharges, suggests that these opioid systems, but not proopiomelanocortin one, may play a role in absence epilepsy.
 ...
PMID:Endogenous opioid peptides in brain and pituitary of rats with absence epilepsy. 163 Jun

The effects of opioid peptides on a 1.1-kb long proopiomelanocortin messenger RNA (POMC mRNA) have been investigated in rat hypothalamic cells maintained in culture. Most opioid peptides exerted an inhibitory control on POMC mRNA steady-state concentrations. beta-Endorphin caused a 65% maximal inhibitory effect (IC50 = 6.1 x 10(-9) M) while slightly less inhibition was caused by Met- and Leu-enkephalin, dynorphin A and DADLE ([D-Ala2,D-Leu5] enkephalin). The effects of beta-endorphin and of Met-enkephalin were completely reversed by the delta opioid antagonist ICI 174,864 while the kappa-receptor specific antagonist binaltorphimine or the sigma-receptor specific antagonist DTG (1,3-di(2-tolyl) guanidine) respectively blocked the inhibitory actions of dynorphin A and of DADLE. The mu-receptor specific agonist DAGO ([D-Ala2,N-Me-Phe4,Gly5-OL]enkephalin) did not affect POMC mRNA levels. The failure of the dopaminergic D2 antagonist haloperidol to modify the inhibitory effects of opioid peptides argues for a direct inhibitory opioid peptide modulation of hypothalamic POMC mRNA levels mediated by the delta-, kappa- and sigma- (but not mu-) receptors in vivo.
 ...
PMID:Regulation of proopiomelanocortin messenger RNA concentrations by opioid peptides in primary cell cultures of rat hypothalamus. 164 65

The effect of opioid neuropeptides was found to be more obvious in functional pathology of the higher nervous activity in hedgehogs. Met-enkephalin exerted a more obvious and longer-lasting effect on complicated forms of nervous activity, particularly inherent those. Naloxone abolished the met-enkephalin effect. The comparative effect of different opioid neuropeptides on inherent and acquired forms of nervous activity in mammals, the correlation between structural distribution of the neuropeptides and their functional properties, are discussed.
 ...
PMID:[The effect of the opioid neuropeptides: met-enkephalin and beta-endorphin on the conditioned reflex activity of hedgehogs]. 166 69

Although the postnatal development of opioid systems of mammalian brain has been well studied, little is known about the ontogeny of and relationship between embryonic (E) opioid peptides and their receptors. Moreover, a simultaneous assessment of levels of the 3 classes of opioid peptides and their putative receptors during embryonal development has not been made. To this end, the ontogeny of opioid peptides and receptors in mouse brain were examined during the period E11.5 to postnatal day 1 (P1). Met-enkephalin, dynorphin and beta-endorphin immunoreactivity were detected before their putative opioid receptors. beta-Endorphin can be discerned as early as E11.5, whereas mu binding was first observed at E12.5. Although dynorphin and Met-enkephalin were measurable at the same time as beta-endorphin, kappa-receptors were not detected until E14.5 and delta sites were not found at all prenatally. Differences in immunoreactivity levels of the 3 peptides occur with dynorphin being lower than Met-enkephalin and beta-endorphin, consistent with a low Bmax for kappa binding. Expression of the 3 opioid peptides as well as mu and kappa opioid receptors rapidly increase in parallel from E14.5 to E18.5. Interestingly, levels of beta-endorphin diminish by P1, the stage at which a sharp rise of mu receptors occurs. In a comparative study of the binding of beta-endorphin 1-31, its truncated form (1-27) and their N-acetyl derivatives to E14.5 brain membranes, beta-endorphin 1-31 exhibited the highest affinity.
 ...
PMID:The prenatal development profile of expression of opioid peptides and receptors in the mouse brain. 167 35

An immunohistochemical study of opioid peptides in the hypophysis of the axolotl, Ambystoma mexicanum, was carried out with antisera against leu-enkephalin, beta-endorphin, met-enkephalin, and dynorphin A (1-8). We found leu-enkephalin immunoreactivity in some fibers of the neural lobe and the median eminence. In contrast to previous reports on mammals and other vertebrates, we found leu-enkephalin immunoreactivity in many cells scattered throughout the anterior lobe. As in other vertebrates, the beta-endorphin immunoreactivity was present in all the cells of the intermediate lobe and in a few cells of the anterior lobe. Met-enkephalin and dynorphin A (1-8) immunoreactivities were only present in the neural lobe and the median eminence. The presence of leu-enkephalin and beta-endorphin in the anterior lobe suggests that these peptides could be acting as hormones released from the hypophysis of the unmetamorphosed amphibian.
 ...
PMID:Evidence for enkephalin- and endorphin-immunoreactive cells in the anterior pituitary of the axolotl Ambystoma mexicanum. 167 48


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>