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 neuroendocrine and neurochemical events which occur in the brain in the context of maternal behaviour fall into two main categories: 1) Those which simultaneously address wide areas of the brain and lack any specific "coding" for maternal behaviour but are nevertheless essential for it to occur. The steroid hormones and rostrally projecting catecholamine systems fall into this category. The steroid hormones may be viewed as primers, but not just for maternal behaviour, while the amines, specifically noradrenaline, act to synchronise a variety of neural systems associated with maternal behaviour. These include the activation of neuroendocrine mechanisms important for the peripheral changes associated with maternal behaviour, an interaction with the oxytocin and beta-endorphin peptidergic systems which are the specific addressing systems, and enhancement of sensory signals and learning contingent upon parturition. Indeed, parturition is the physiological event which activates the noradrenergic system in the context of maternal behaviour. 2) Those which address restricted areas of the brain and may be viewed as specific to maternal behaviour. Their action is dependent on estrogen priming and the noradrenergic synchronisation of other neural events in order for complete maternal behaviour to ensue. The oxytocinergic and beta-endorphin peptidergic systems fall into this category, promoting maternal behaviour and the neural reinforcement associated with this. In order to ensure specificity, these peptidergic systems may be inhibitory to potentially competing behaviours such as sexual behaviour and the reproductive neuroendocrine response associated with it. Although not discussed in this review, the nigrostriatal dopamine projection may be considered both specific, in that it relates only to motor events, and non-specific, in that this relationship exists in all behavioural contexts. Finally, as maternal behaviour progresses, other parts of the brain are called upon to coordinate the different behaviours that become associated with maternalism and ensure protection and feeding of the offspring. The suckling stimulus appears to be important for activating these neural systems by way of the peripeduncular nucleus.
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PMID:Central mechanisms underlying the neural and neuroendocrine determinants of maternal behaviour. 289 99

This study was undertaken to examine short photoperiod (SD; 8 h of light, 16 h of darkness)-induced alterations in reproductive endocrine and neuroendocrine parameters in the male white-footed mouse, Peromyscus leucopus. Exposure to SD for 8 weeks caused dramatic reductions in testis and seminal vesicle weights, decreased circulating LH and testosterone levels, and lowered the content of LH in the pituitary gland relative to those in mice under long photoperiod (LD; 16 h of light, 8 h of darkness). These changes were associated with significant increases in content of radioimmunoassayable GnRH in the mediobasal hypothalamus (MBH) and anterior hypothalamus at two time points in the light/dark cycle: 2100 h (dark phase) and 0900 h (light phase), respectively. Exposure to SD also caused an increase in radioimmunoassayable beta-endorphin in the MBH and preoptic area of the hypothalamus (POA) at 2100 h, but not at 0900 h. Mice exposed to SD also had a significantly higher metabolism of serotonin in the MBH at 0900 and 2100 h compared to mice under LD. The concentration of noradrenaline in the hypothalamus was unaffected by exposure to SD. However, the metabolism of dopamine (DA) in the POA at 0900 h was significantly increased relative to that in mice maintained under LD at this time. This increase in DA metabolism was associated with enhanced immunocytochemical staining for tyrosine hydroxylase in nerve fibers of the POA. Conversely, staining for tyrosine hydroxylase in tuberoinfundibular DA cell bodies of the arcuate nucleus was less intense under SD exposure. From these data it is concluded that exposure to SD caused regional and time-dependent alterations in the activities of hypothalamic amines (serotonin and DA) and neuropeptides (beta-endorphin and GnRH). These changes may be part of the neuroendocrine mechanism for SD-induced seasonal adaptations.
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PMID:Photoperiodic adjustments in hypothalamic amines, gonadotropin-releasing hormone, and beta-endorphin in the white-footed mouse. 289

To further our understanding of the functional role of catecholaminergic systems in regulating hypothalamic corticotropin-releasing hormone (CRH) secretion, we assessed the direct effects of a multiplicity of catecholamine agonists and antagonists on hypothalamic CRH secretion. To accomplish this, we used an in vitro rat hypothalamic organ culture system in which CRH secretion from single explants was evaluated by a specific RIA (IR-rCRH). Norepinephrine (NE) stimulated IR-rCRH secretion dose dependently, with peak effects in the nanomolar range. The effect of NE was antagonized by the mixed alpha antagonist phentolamine, the alpha 1 antagonist prazosin, and the alpha 2 antagonist yohimbine, but not by the beta blocker, L-propanolol. Compatible with these data were the findings that the alpha 1 agonist phenylephrine and the alpha 2 agonist clonidine both stimulated IR-rCRH secretion in a dose-dependent fashion. On the other hand, whereas the beta agonist, isoproterenol, caused a weak, non-dose-dependent increase in IR-rCRH secretion, this effect could not be antagonized by L-propanolol. Despite pretreatment with serotonin and acetylcholine antagonists, the effect of NE upon IR-rCRH secretion was undiminished, suggesting that NE-induced CRH secretion is not mediated by either neurotransmitter. On the other hand, pretreatment with gamma-aminobutyric acid (GABA) attenuated NE-induced IR-rCRH secretion. Whereas epinephrine (E) stimulated IR-rCRH secretion, this occurred only at higher concentrations, and was antagonized by phentolamine, but not by L-propanolol. Dopamine (DA) had a weak stimulatory effect that could be antagonized by the DA1 receptor antagonist, SCH 23390, but not by phentolamine. We conclude that NE and E stimulate hypothalamic IR-rCRH secretion via alpha 1 and alpha 2 receptors. The effect of NE upon IR-rCRH secretion is not apparently mediated by serotonergic or cholinergic interneurons, but is modulated by the inhibitory neurotransmitter, GABA. These data support the idea that the central catecholaminergic systems are excitatory rather than inhibitory upon CRH secretion when acting directly at the hypothalamic level.
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PMID:Catecholamine effects upon rat hypothalamic corticotropin-releasing hormone secretion in vitro. 290 33

The aim of the study was to evaluate full-thickness and partially stripped jejunum as a model for neurogenic control of electrogenic ion transport. The electrical properties of full-thickness and partially stripped segments were studied in Ussing chambers. Using square-pulse analysis, subepithelial and epithelial resistances (Rs and Rp) were determined, and by compensating for the potential fall across Rs, the current generated by the epithelium could be measured. In full-thickness tissue, Rs was approximately 80% of total tissue resistance, and the current measured during short-circuiting of the whole tissue (SCC) was therefore only 20-25% of the current generated by the epithelium (Im). Surgical stripping of the tissue decreased Rs by 10-20%. This means that in full thickness as well as in stripped tissue, 70-80% of the potential difference across the epithelial layer remains after traditional 'short circuiting'. Over a 25-min period, none of the electrical parameters changed significantly in the full-thickness tissues. In the stripped group PD, SCC and Im fell significantly, and in parallel during the same period of time. Neither glucose, noradrenaline, met-enkephalin or carbachol had any significant effect on Rs, Rp or the Rs/Rp ratio. The relative effects of these agents on Im and SCC were therefore similar. Substance P and VIP increased the Rs/Rp ratio significantly and, therefore, the effect of these drugs on Im was significantly more pronounced than the effect on SCC. The results show that the subepithelial resistance must be taken into account when the electrogenic activity in the epithelium is to be determined correctly. Conventionally measured SCC reflects the electrogenic effect of the tested putative neurotransmitters, but the magnitude of the responses is grossly underestimated, particularly for substance P and VIP.
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PMID:The importance of the subepithelial resistance for the electrical properties of the rat jejunum in vitro. 290 29

Seventeen human subjects fasted without electrolyte replacement for 3 days and hormone levels were measured before, during and after the fast. Immediate consequences of the fasting state in healthy human subjects include a marked increase in plasma cortisol. ACTH, beta-endorphin, beta-lipotrophic hormone, adrenaline, noradrenaline and dopamine. Levels of all these hormones were much greater on the first morning of the fast than in the post-prandial state, even though the plasma glucose level was no lower than that observed on the morning before the fast began. A clear fall in TSH and tri-iodothyronine (T3) levels was observed, but thyroxine levels did not change significantly. Insulin levels fell whereas proinsulin levels did not fall during the fast, though they did rise markedly upon re-feeding. An increase in GH levels was particularly apparent in male subjects, but was also seen in females when evening samples were compared. Pancreatic glucagon showed a modest rise during the fast, but fell again on refeeding; total glucagon also rose as the fast proceeded, but increased markedly upon re-feeding. Levels of gastrin and peptide YY remained low during the fast. Plasma electrolyte levels were unchanged. The following were closely correlated: cortisol with ACTH, T3 with log10 TSH, dopamine with noradrenaline, and (negatively, during the fast) pancreatic glucagon with glucose.
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PMID:The effect of a 72-h fast on plasma levels of pituitary, adrenal, thyroid, pancreatic and gastrointestinal hormones in healthy men and women. 292 6

The effects of pretreatment of rats with an intrahypothalamic injection of 6-hydroxydopamine on the thermal responses induced by intrahypothalamic injection of noradrenaline, prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin were assessed. Administration of either noradrenaline (2-10 micrograms), prostaglandin E2 (10-40 ng), thyrotropin-releasing hormone (0.5-2.0 micrograms) or beta-endorphin (1-3 micrograms) into the preoptic anterior hypothalamus caused a dose-dependent rise in rectal temperature in conscious rats at an ambient temperature of 22 degrees C. In addition, it was found that three intrahypothalamic doses of 10 micrograms of 6-hydroxydopamine at intervals of 2 days caused a significant depletion of noradrenaline in the hypothalamus to 26.4% of control while the concentration of dopamine in the hypothalamus was not significantly reduced at 95.3% of control. Furthermore, the hyperthermic responses induced by prostaglandin E2, thyrotropin-releasing hormone, or beta-endorphin were greatly attenuated after selective depletion of noradrenaline in the hypothalamus in rats. However, selective depletion of noradrenaline did not affect the noradrenaline-induced hyperthermic responses. The data indicate that either prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin may act through the endogenous release of noradrenaline from the hypothalamus to induce hyperthermic responses in rats.
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PMID:Depletion of noradrenaline in the hypothalamus reduces the febrile responses induced by prostaglandin E2, thyrotropin-releasing hormone and beta-endorphin in rats. 293 40

Cord plasma levels of endorphins and catecholamines were correlated with the values of cord blood gas analysis and with hemodynamic parameters in 11 newborns (group A) delivered by elective cesarean section and in 18 newborns (group B) born spontaneously by vaginal route. All infants were in a good condition. No statistically significant differences were found in the mean cord plasma levels of adrenaline (A), noradrenaline (NA) and immunoreactive beta-endorphin (ir beta-E) between groups A and B. After spontaneous labor in group B a highly significant negative correlation was found between plasma NA level and pH and a positive correlation between NA and carbon dioxide tension in cord arterial blood and between NA and the short-term variability of the fetal heart rate before birth. Cord plasma A and ir beta-E did not show such correlations. These findings show that cord plasma level of NA is a sensitive indicator of minor stress during normal labor. After birth, during the first two hours of life, the mean plasma level of ir beta-E decreased in group B after vaginal delivery, but remained at a higher level in group A after elective cesarean section. This shows that the mode of delivery influences the neonatal endorphin secretion.
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PMID:Stress of delivery and plasma endorphins and catecholamines in the newborn infant. 293 59

Growing evidence indicates that most patients with coronary artery disease frequently have episodes of painless myocardial ischemia. Previous studies from our institution show that the severity and duration of myocardial ischemia are necessary but not sufficient factors to explain the occurrence of anginal pain. The responses to a battery of painful stimuli were studied in 12 patients with predominantly painless (group A) and in 15 patients with predominantly painful (group B) ischemic episodes. The severity of myocardial ischemia as assessed by the measurement of ST-segment depression during exercise stress testing and during ambulatory electrocardiographic monitoring was comparable in the 2 groups. Patients in group A had a significantly higher threshold and tolerance for forearm ischemia (+32%, p less than 0.05; +120%, p less than 0.001), cold (+100%, p less than 0.05; +180%, p less than 0.01) and electrical skin stimulation (+145%, p less than 0.01; +109%, p less than 0.01), but the overlap between the 2 groups was often appreciable. In the 6 patients with the longest tolerance times for forearm ischemic pain (all in group A) and in the 5 having the shortest tolerance times (all in group B), plasma levels of beta endorphin, met-enkephalin, noradrenaline and adrenaline were similar during both the basal state and the induction of forearm ischemic pain. Thus, a generalized defective perception of painful stimuli plays an important role in many patients with predominantly painless myocardial ischemia. Other mechanisms, however, may also be important, particularly in patients whose threshold and tolerance values overlap with those of patients who have predominantly painful myocardial ischemia.
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PMID:Importance of generalized defective perception of painful stimuli as a cause of silent myocardial ischemia in chronic stable angina pectoris. 294 17

1 Intracarotid injection of [Leu]enkephalin and [Met]enkephalin produced a dose-dependent biphasic change in blood pressure of the rat consisting of an initial shortlasting fall followed by a longlasting increase of blood pressure. Naloxone consistently depressed or abolished the effects of enkephalins on blood pressure. 2 Intracarotid injection of beta-endorphin only occasionally produced a hypotension, or did not produce any change in the blood pressure of the rat. 3 All three opioids ([Leu]enkephalin, [Met]enkephalin and beta-endorphin) significantly depressed or abolished the hypertensive response to intravenous injection of physostigmine. This depressive action of opioids was easily reversed by naloxone. 5 It is concluded that opioids depress the central cholinergic link implicated in the hypertensive response to physostigmine most probably by inhibiting acetylcholine and/or noradrenaline release in the structures relevant for the action of physostigmine on blood pressure of the rat. This interaction is realized through the activation of opioid receptor(s).
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PMID:The effect of enkephalins and of beta-endorphin on the hypertensive response to physostigmine in the rat. 295 44

Studies of the roles played by neurotransmitters in the development of hypertension in the spontaneously hypertensive (SHR) rat are complicated by the presence of genetic differences between SHR and normotensive control rats, which are not related to differences in blood pressure. One approach that may be used in an attempt to overcome this difficulty is to study the manner in which neurotransmitter and metabolite levels change with age, and to relate these changes to alterations in blood pressure with ageing. Noradrenaline (NA) levels in the brainstem and spinal cord of SHR and Wistar Kyoto rats fell with age, while 3,4-dihydroxyphenylethyleneglycol (DHPG) levels (a neuronal metabolite of noradrenaline) remained constant. Similar changes were seen when NA and DHPG levels were measured in the discrete brainstem A1, A2, and C2 region, and when adrenaline, NA, and DHPG levels were examined in the C1 region. Differences in age-related changes of neuropeptide Y (NPY) levels were also found in the ventromedial nucleus of the hypothalamus and the locus coeruleus, and of beta-endorphin in the anterior hypothalamic nucleus, the paragigantocellular nucleus of the brainstem, and the locus coeruleus. These changes may indicate either a progressive increase in the activity of neurons in the sympathoexcitatory C1 region or a progressive reduction in the activity of vasodepressor A1, A2, and C2 regions with ageing, or both. However, changes in catecholamines and metabolites with age were similar in both strains and therefore cannot readily explain the more rapid rise in blood pressure with ageing in SHR rats.
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PMID:Neurotransmitters and neuropeptides in blood pressure regulation in the spontaneously hypertensive rat. 296 19


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