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)

Autonomic dysfunction, including arrhythmias, has been shown to be associated with epileptogenic activity. This study examines the potential role for enkephalins in this process. A long lasting elevation of immunoreactive methionine (met)-enkephalin content in the septum, hypothalamus, amygdala, and hippocampus of rats occurs after pentylenetetrazol-induced convulsions (Brain Research 297: 121-125, 1984). Brennan et al (Life Sciences 27: 1097-1101, 1980) reported a greater percent inhibition of potassium-stimulated GABA release with increasing concentrations of met-enkephalin. Snead and Bearden (Science 210: 1031-1033, 1980) found that leucine-enkephalin in the central nervous system may induce epileptogenic activity. In addition, (d-alanine2) met-enkephalin has been shown to produce a centrally mediated vasopressor response as well as attenuation of the baroreceptor reflex in conscious cats (Hypertension 3: 395-407, 1981), possibly leading to autonomic imbalance. The latter may precipitate arrhythmias and sudden unexplained death in the epileptic patient. Resolution of the question of whether enkephalins elicit epileptogenic activity and autonomic dysfunction via inhibition of GABA release is important since an understanding of this mechanism should eventually allow the design of pharmacologic agents to prevent the epileptogenic activity, autonomic dysfunction and the associated sudden death.
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PMID:The role of enkephalins in the production of epileptogenic activity and autonomic dysfunction: origin of arrhythmia and sudden death in the epileptic patient? 361 1

The GABAergic regulation of proopiomelanocortin messenger RNA (POMC mRNA) levels in rat pituitary was investigated using molecular hybridization of DNA complementary to POMC mRNA. Endogenous GABA levels increased, in vivo, by inhibiting the GABA catabolic enzyme GABA-transaminase (GAT) with ethalonamine-O-sulfate (EOS) or with vinyl-GABA (VG). Rats were treated with VG (100 mg/kg or 800 mg/kg) or EOS (100 mg/kg), administered each second day. GABA levels in the neurointermediate lobe (NIL) and anterior lobe (AL) of the hypophysis and in the hypothalamus were significantly increased following 4 days of VG treatment (800 mg/kg). All treatments resulted in a 40-60% decrease in POMC mRNA levels after 4 days in the NIL but not in the AL. A similar decrease of about 60% in POMC mRNA levels in the NIL was seen when EOS was given in the drinking water (5 mg/ml). In this set of experiments the time course of alteration of POMC mRNA in the NIL and the concentration of alpha-MSH, a POMC-derived peptide, were analysed. After one day of EOS treatment, when POMC levels had already decreased by 40%, alpha-MSH levels were significantly elevated (34% above controls), possibly reflecting an inhibition of alpha-MSH secretion. However, after 4 and 8 days, POMC mRNA levels and tissue alpha-MSH levels had significantly decreased. When tested in vitro, on primary cultures of IL cells, GABA (10 microM) reduced POMC mRNA levels by 40% after 3 days of treatment. These results show that GABA exerts a direct inhibitory effect on POMC gene expression in the intermediate lobe.
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PMID:GABA differentially regulates the gene expression of proopiomelanocortin in rat intermediate and anterior pituitary. 373 46

Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.
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PMID:[Neuroendocrinologic aspects of epilepsy]. 609 64

The effects of drugs on the K+-evoked release of met-enkephalin from superfused rat striatal slices were investigated using a specific radioimmunoassay. GABA, at concentrations of 50 microM and 100 microM, and the GABA agonist muscimol (50 microM), significantly inhibited the release. The inhibitory effect of GABA was reversed by picrotoxin suggesting that GABA inhibition is mediated by GABA receptors. Selected concentrations of the dopamine agonists apomorphine and ergonovine, as well as of haloperidol, acetylcholine, carbachol, noradrenaline, glutamic acid and substance P, had no effect on the release of metenkephalin. Increases in the evoked release (80%) and striatal enkephalin content (60%) were found in rats after chronic haloperidol administration, pointing to an increase in the synthesis and utilization of striatal enkephalin. No differences were found between the release from slices from morphine-tolerant/dependent and naive rats or after addition of naloxone to slices derived from tolerant/dependent animals. Selected concentrations of morphine and naloxone had no effect on release suggesting the absence of a mechanism for the regulation of enkephalin release involving autoreceptors.
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PMID:K+-evoked release of met-enkephalin from rat striatum in vitro: effect of putative neurotransmitters and morphine. 610 16

It is well known that the release of melanocyte-stimulating hormone (MSH) from the pituitary gland is mainly controlled by an inhibitory influence from the hypothalamus. In addition to this inhibitory control, there may also be a stimulatory influence. Most, but by no means all, of the evidence is compatible with the possibility that inhibition is mediated by dopaminergic and/or alpha-adrenergic receptors. Gamma-aminobutyric acid also has been shown to have an inhibitory role in some studies. beta-Adrenergic receptors, serotonin, and acetylcholine may be involved in the stimulation of MSH release. Interaction of hypothalamic peptides like Pro-Leu-Gly-NH2(MIF-I) with biogenic amines, however, has not been excluded as a factor in the control of the release of MSH from the pituitary. Just as the evidence for the involvement of amines in the control of MSH release is somewhat puzzling and contradictory, conflicting evidence concerning their involvement in mediating the specific effects of MSH and MIF-I on the CNS remains unresolved.
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PMID:Possible aminergic mediation of MSH release and of the CNS effects of MSH and MIF-I. 610 77

[3H]-Dopamine was found to be released from the rabbit retina in vitro by light stimulation, by 40 mM K+, and by alpha-MSH (alpha-Melanocyte-Stimulating Hormone) down to about 10(-7) M. The effect of alpha-MSH was dose-dependent. A number of known and putative retinal neurotransmitters and agonists (GABA, muscimol, glutamic acid, kainic acid, glycine, and carbachol, all 10(-4) M) were without significant effect. The results show that it is unlikely that there are excitatory receptors on the retinal dopaminergic neurons to any of the conventional transmitters. Further, alpha-MSH seems of interest as a possible neuroactive retinal substance, which was previously not been suspected.
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PMID:[3H]-dopamine release from the rabbit retina. 611 Dec 60

Our presently somewhat limited knowledge of the modulation of the content, release and turnover of endorphins in brain and pituitary by acute and chronic drug treatment is reviewed and discussed particularly in relation to the problem of addiction. In vitro studies in striatal slices and isolated anterior and intermediate/posterior lobes of the pituitary point to the existence of specific interactions between endorphins and neurotransmitters. In vivo studies have revealed acute GABA-mediated effects of benzodiazepines upon striatal levels of met-enkephalin activity. Morphine exerts no acute effects upon endorphin levels, but decreases the levels of particular endorphins in specific areas of brain and pituitary after long-term treatment; somewhat similar effects are observed after prolonged intake of ethanol, whereas chronic haloperidol treatment results in an increase in levels of endorphins in brain and pituitary. Incorporation studies employing the intermediate/posterior lobe of the pituitary have revealed that the changes in beta-endorphin levels produced by prolonged treatment with morphine or haloperidol reflect a respective depressed or enhanced synthesis of the beta-endorphin precursor pro-opiocortin, whilst the enzymatic processing of this precursor remains unmodified. Studies in cell-free preparations demonstrated that m-RNA extracted from the intermediate/posterior lobes of chronically morphinized rats possesses a decreased "activity".
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PMID:Pharmacological modulation of opiate-like peptide systems. 611 2

The release of immunoreactive Met-enkephalin (I-ME) from the rat striatum was studied in vitro using a batch technique. A basal release of the order of 2-3% of total I-ME tissue content per 10 min was found. Both dipeptides kyotorphin and D-kyotorphin produced equipotently dose-dependent I-ME release, with 0.5 mM maximal concentration causing 2-3-fold stimulation of release. This release was calcium-dependent. In concentrations up to 1 mM both dipeptides did not change the basal release of [3H]noradrenaline, [3H]GABA, [3H]D-aspartate and immunoreactive beta-endorphin from various brain structures. The results support a role of kyotorphin as a specific I-ME-releasing factor in the rat brain.
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PMID:Kyotorphin and D-kyotorphin stimulate Met-enkephalin release from rat striatum in vitro. 614 36

Gamma-aminobutyric acid (GABA) blocked concentration of the pigments in melanophores and erythrophores of intact crabs. GABA blocked the release of pigment concentrating hormones from the isolated eyestalk. Octopamine (OA) blocked black pigment dispersion in intact crabs, but did not affect red pigment dispersion or concentration. OA blocked the release of black pigment dispersing hormone from isolated eyestalks. Met-enkephalin, but not Leu-enkephalin, stimulated black and red pigment concentration in intact crabs. Met-enkephalin, but not Leu-enkephalin, stimulated the release of pigment concentrating hormones from isolated eyestalks. Naloxone blocked the effects of Met-enkephalin in intact crabs and on isolated eyestalks. Beta-endorphin induced black pigment dispersion in intact crabs and in isolated legs.
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PMID:Regulation of neurohormone release in the fiddler crab, Uca pugilator: effects of gamma-aminobutyric acid, octopamine, Met-enkephalin, and beta-endorphin. 614 82

Intracerebroventricular administration of muscimol, a potent GABA-receptor agonist, counteracted the antinociceptive effect of morphine or beta-endorphin in rats as measured by the "tail flick" method. Muscimol's activity was reversed by bicuculline. Isoguvacine, another GABA agonist, as well as nipecotic acid and guvacine, two inhibitors of neuronal and glial uptake of GABA, also antagonized morphine's antinociceptive effect. A role of the central GABA-ergic system in mediating opiate antinociception is proposed.
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PMID:Effects of some GABA-mimetic drugs on the antinociceptive activity of morphine and beta-endorphin in rats. 626 10


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