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 level of opioid peptides: beta-endorphin and dynorphin, binding to the mu and kappa opioid receptors and the analgesic response of those endogenous opioid systems to stress were investigated in two strains of mice: C57BL/6 (C57) and DBA/2 (DBA). The nociceptive threshold of DBA mice was higher than that of C57 mice. KD values for spinal mu receptors were lower in C57, while KD for cerebral kappa receptors were higher in this strain. DBA mice have significantly higher concentrations of dynorphin in the hypothalamus and neurointermediate lobe of the pituitary. Stress-induced analgesia was much greater in C57 than in DBA mice. In the hypothalamus both stress procedures depressed the concentrations of beta-endorphin in C57, and dynorphin in DBA mice. The level of beta-endorphin increased in the neurointermediate lobe in C57 and in anterior lobe of the pituitary in DBA mice. In the spinal cord both stress procedures depressed the dynorphin level. The above data indicate that C57 and DBA mice differ in the endogenous opioid peptide content, stress-induced alteration and opioid receptor affinity, the effects which might correlate with their different responses to environmental factors and pharmacological agents.
Pol J Pharmacol Pharm
PMID:The difference in stress-induced analgesia in C57BL/6 and DBA/2 mice: a search for biochemical correlates. 290 36

Beta-endorphin concentrations were determined in the cerebrospinal fluid and blood before and after lumbar tap in 19 patients with lumbosacral pains. No statistically significant difference was observed in this concentration before and after lumbar tap, although in individual cases a significant rise of beta-endorphin occurred. The mean beta-endorphin concentration in blood was about twice as high as in the cerebrospinal fluid. No correlation was noticed between the concentration of beta-endorphin in blood and in CSF.
Neurol Neurochir Pol
PMID:[Beta-endorphin levels in the blood and cerebrospinal fluid in humans]. 293 69

A local injection of kainic acid (KA) into the dorsal raphe nucleus (NRD) increased the motor activity and produced head shakes, hind limb abduction, forepaw treading and sniffing. This syndrome was antagonized partly by cyproheptadine and completely by naloxone. An injection of KA into the median raphe nucleus (NRM) produced sedation, catalepsy and analgesia, which were accompanied by a decrease in the beta-endorphin immunoreactivity in the mesencephalon. Naloxone completely reversed the behavioral inhibition after KA injections into the NRM, while a pretreatment with cyproheptadine augmented the catalepsy. KA injected into the NRD and NRM depressed the forebrain level of serotonin and slightly elevated that of 5-hydroxyindoleacetic acid. The results demonstrate that besides serotonin the opioid system is also involved in various effects induced by activation of the raphe nuclei.
Pol J Pharmacol Pharm
PMID:Different behavioral responses of rats to kainate injections into the dorsal and median raphe nuclei. 295 46

Brain enzymes convert the opioid peptide beta-endorphin (beta E-(1-31)) to alpha- and gamma-endorphin and to several non-opioid fragments by further cleavage of the tyrosine residue or acetylation. Several of these peptides selectively affect brain functions. alpha-Endorphin (beta E-(1-16)) and relate non-opioid fragments (beta E-(2-16), beta E-(2-9) a.o.) like amphetamine, delay extinction of pole-jumping avoidance behavior and facilitate passive avoidance behavior. In addition these peptides enhance the stereotyped sniffing response induced by the injection of apomorphine into the nucleus caudatus. The fragment beta E-(10-16) inhibits, like serotonin and antidepressants, the behavioral effects of melatonin injected into the nucleus accumbens. gamma-Endorphin (beta E-(1-17)) has inherent opioid and neuroleptic-like properties, e.g. demonstrated by a naloxone reversible inhibition of hypermotility induced by apomorphine following injection into the nucleus accumbens. Also the non-opioid gamma-type endorphins (e.g. DT gamma E (beta E-(2-17) and DE gamma E (beta E-(6-17)) mimic certain effects of neuroleptics. These peptides facilitate extinction of pole-jumping avoidance behavior, attenuate passive avoidance behavior and antagonize the hypomotility and stereotyped sniffing induced by apomorphine injected into the nucleus accumbens and pyriform cortex respectively. These and other behavioral studies, including grasping responses, brain stimulation reward, food and other positively rewarded behavior, indicate that the action of alpha-type endorphins is in some aspects comparable to that of psychostimulants, while the effects of gamma-type endorphins are comparable to those of classical as well as atypical neuroleptics. Indeed, gamma-type endorphins have antipsychotic effects in a category of schizophrenic patients.
Pol J Pharmacol Pharm
PMID:Non-opiate effects of neuropeptides derived from beta-endorphin. 297 64

Degradation of iodinated beta-endorphin in human and rat plasma was investigated, using different proteinase inhibitors. This degradation affects the radioimmunoassay quality. Additional blank tubes were also prepared during assay procedure to avoid the effect of 125-I-beta-endorphin adsorption on the dextran-coated charcoal in the presence and absence of plasma proteins, what avoids underestimation of the beta-endorphin level in plasma samples. Based on the above observations, the sensitive and direct radioimmunoassay of beta-endorphin was developed in human and rat plasma.
Pol J Pharmacol Pharm
PMID:Degradation of the labelled beta-endorphin is an important factor of direct RIA in the human and rat plasma. 297 34

New syntheses of three thyrotropin releasing hormone (TRH) analogues ([Dopa2]THR, [Nic1]TRH, and [Tyr(30NO2)2]TRH) have been reported (Dopa stands for L-3,4-dihydroxyphenylalanine, Nic--for nicotinic acid and Tyr(3-NO2)--for L-3-nitrotyrosine). These three TRH analogues and five already known ones ([Aad1Tca3]TRH, [D-His2]TRH, [D-Pro3]TRH, [Pro-NH-NH2(3)]TRH and [Tyr2]TRH), were studied in vitro for their binding activity to rat pituitary TRH receptors and a-MSH releasing activity in the neuro-intermediate lobe of frogs. Competition of analogues for 3H-TRH binding to rat anterior pituitary membrane fraction was used. One of ten tested analogues ([Aad1, Tca]3 TRH) was as potent as TRH in competing for high-affinity binding sites (Kd = 8.5 nM). The binding activity of diastereoisomers ([D-His2]TRH and [D-Pro3]TRH) was reduced as well as that of analogue [Pro-NH-NH2(3)]TRH. The rest of the analogues were inactive. The binding activities were in good accordance with alpha-MSH releasing activities.
Pol J Pharmacol Pharm
PMID:Synthesis, receptor binding affinities and alpha-MSH releasing activities of TRH analogues. 299 54

In 1984 and at the beginning of 1985 the authors carried out radioimmunoassays (SORIN-CIS kit) the plasma levels of ACTH in 116 multiple sclerosis patients (m-52, f-64) and in 10 cases this radioimmunoassay was done in the cerebrospinal fluid (m-5, f-5). The control group comprised 90 patients with ischialgia and neuroses. The normal value in the plasma was from 0 to 80.86 pg/ml, and in the fluid it was from 0 to 77.08 pg/ml. In multiple sclerosis patients the plasma ACTH level was from 0 to 286.9 pg/ml, in the cerebrospinal fluid from 0 to 89 pg/ml. The values of ACTH were significantly higher in multiple sclerosis patients, mainly in males. In the fluid the level of ACTH was significantly higher in the studied patients. No significant differences in ACTH levels were found between males and females with multiple sclerosis, and in the control group this level was higher in females. Raised ACTH level was found mainly in multiple sclerosis with lung duration of the disease (10 years) at the time of exacerbations. The authors continue studies on the axis hypothalamus-hypophysis-adrenals, on various hormones, prostaglandins, beta-endorphin, biochemical markers, cAMP, cCMP, arylosulphatase A and B MBC etc.
Neurol Neurochir Pol
PMID:[ACTH in the plasma and cerebrospinal fluid in patients with multiple sclerosis]. 303 9

D-Met2, Pro5-enkephalinamide (DMPEA) is an opioid peptide having analgesic activity in animals more potent after intravenous administration than morphine. It is less toxic but in animals it showed a higher dependence capacity than morphine. Besides analgesia DMPEA produces in rodent behavioral symptoms similar to those evoked by morphine or beta-endorphin, resembling the actions of neuroleptica. In human trials DMPEA was found to produce unpleasant sensations, no euphoria, and sometimes even dysphoria. DMPEA increases the serum levels of prolactin, growth hormone and, to a less extent, of TSH. Those effect of DMPEA on pituitary hormones. Finally, the human studies indicated that DMPEA antagonized pain (measured with the submaximum effort tourniquet technique), but did not affect adversely and even improved attention and short-term memory; it had no effect on the long-term memory. As the subjective effects of DMPEA are not pleasant, and no patient desired to obtain another treatment, some optimism as to low habit-forming properties of DMPEA may be justified.
Pol J Pharmacol Pharm
PMID:Pharmacological and human studies with a highly potent opioid peptide, D-Met2, Pro5-enkephalinamide. 333 15

The authors determined in 1984 by radioimmunoassay (INEP kit) the serum prolactin concentration in 76 multiple sclerosis patients (33 males and 34 females) aged from 21 to 53 years, with disease duration from 2 to 30 years. The control group comprised 110 healthy subjects. Normal prolactin values were 150-750 mIU/ml in females and 150-500 mIU/ml in males. In about one-third of the patients raised prolactin level was found which failed to correlate with the age of the patients and with increased beta-endorphin level in them. The authors suppose that hyperprolactinaemia may be of importance in certain clinical signs of multiple sclerosis. Further investigations on prolactin are conducted with reference to the circadian rhythm of prolactin secretion and dynamic tests.
Neurol Neurochir Pol
PMID:[Prolactin in the blood serum of patients with multiple sclerosis]. 367 May 26

The lesions of medial habenular nuclei increased the pain sensitivity, enhanced the analgesic activity of morphine and slightly activated the behavior. The lesion of fasciculus retroflexus, a pathway connecting habenular nuclei with interpeduncular nucleus enhanced the pain sensitivity less markedly, did not change the efficacy of morphine analgesia, but significantly increased the activity of animals. The lesion of interpeduncular nucleus influenced the pain sensitivity to a smallest degree, did not change the analgesic activity of morphine, but dramatically increased the activity of animals. The activation did not resemble the aimless excitation of amphetamine-treated or raphe-lesioned rats, and no signs of increased emotionality or irritability were noted. The results are interpreted as an evidence of habenulo-interpenduncular complex being a part of a system, involved in the regulation of behavioral activity and the sensitivity to the aversive stimuli. These functions are in all probability mediated partly through substance P and met-enkephalin containing neurons, present in these structures.
Pol J Pharmacol Pharm
PMID:Habenulo-interpeduncular lesions: the effects on pain sensitivity, morphine analgesia and open-field behavior in rats. 390 26


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