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)

Two cases of hypothalamic hamartoma are presented. The first patient was a 4-year-old boy with precocious puberty, and the second was a 6-year-old boy with epileptic seizures. In both patients, clinical symptoms and signs appeared at the age of 2 years and progressed thereafter. Computerized tomography and magnetic resonance imaging in both cases disclosed a suprasellar mass lesion in continuity with the hypothalamus. Removal of the lesions affected the endocrinological status and/or seizure control. Pathological examination revealed the lesions to be composed of well-differentiated neuronal and glial cells. Immunohistochemical study demonstrated the presence of beta-endorphin, corticotropin-releasing factor, oxytocin, and neurofilament protein (210 kD) in the neuronal cells of the first patient, but no neuropeptides were detected in the second. Electron microscopic examination on the second patient disclosed the presence of many nonmyelinated and some myelinated neuronal processes containing dense-core and clear vesicles. The morphological characteristics and the role of surgery for this lesion are discussed.
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PMID:Hypothalamic hamartoma. Report of two cases. 292 5

The localization of opioid peptides in the rat hippocampal formation and the epileptogenic action of beta-endorphin and certain enkephalin analogues have led to speculations that opioids may play a role in limbic seizures. These immunochemical and electroencephalographic data are compatible with single-unit electrophysiological studies showing predominant excitations of hippocampal pyramidal neurons in CA1 and CA3 fields produced by iontophoresis of endorphins or enkephalins. These excitations are naloxone sensitive and appear to arise from a disinhibitory mechanism due to inhibition of inhibitory interneurons. Thus, intracellular recordings in in vitro preparations of hippocampus usually show opioid-induced reduction of inhibitory postsynaptic potentials. However, more recent studies suggest that a major opioid-containing pathway in the hippocampus, the mossy fiber projection from the dentate gyrus to CA3 pyramidal neurons, contains more pro-dynorphin-derived peptides than pro-enkephalin. Intracerebroventricular dynorphin does not induce epileptiform activity in the rat, and single-unit and field-potential studies show mixed effects on CA3 neuronal excitability, with more inhibitory responses than are seen with the enkephalins. Selective inactivation of mu opioid receptors reveals that dynorphin, which was previously shown to express specificity for kappa receptors, can act on delta receptors in CA1. Furthermore, a specific kappa agonist, U50,488H, has inhibitory actions when applied directly to CA3 neurons. These data suggest the presence of multiple opioid receptor types in the hippocampus. These multiple receptors may point to heterogeneous functions of the different families of opioid peptides in various regions of the hippocampus, and could explain the divergent effects reported for the various opioids and naloxone to promote or prevent paroxysmal activity.
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PMID:Opioid peptides and epileptogenesis in the limbic system: cellular mechanisms. 293 97

The effects of single and repeated electroconvulsive treatment (ECT) on beta-endorphin (beta-EP), cortisol, growth hormone (GH) and prolactin (Prl) plasma levels were investigated in nine depressed patients. Blood samples were monitored a day before ECT, the day of the first and sixth ECT (0, 30, 60 and 90 min after seizures), the day afterwards and 4 weeks after termination of the ECT course. A significant elevation of beta-EP levels was achieved immediately with and 24 h after the first and the sixth ECT. A transient increase in basal beta-EP was observed 1 day following the sixth ECT in comparison with pre-treatment level. Peak and 30 min levels of cortisol were increased compared with baseline by the first ECT. The former (peak) but not the latter (30 min) were increased also at the sixth treatment. GH levels were decreased the day after the first ECT in comparison with the pre-treatment levels and immediately following each ECT in comparison with baseline. A trend toward elevation of Prl was observed immediately after the first and sixth ECT, although the rise did not reach significant levels. ECT administration stimulated beta-EP and cortisol secretion and suppressed human GH release, possibly by activation of endorphinergic and/or serotonergic systems. These mechanisms might be involved in the beneficial effect of ECT in depression.
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PMID:The effect of acute and repeated electroconvulsive treatment on plasma beta-endorphin, growth hormone, prolactin and cortisol secretion in depressed patients. 295 20

The effects of nicotine on secretion of the pituitary peptides beta-endorphin, alpha MSH, and ACTH were studied using the isolated perfused mouse brain (IPMB) and isolated superfused pituitaries of C3H mice. Nicotine (6.1 microM) stimulated secretion of beta-endorphin immunoreactivity from C3H IPMB approximately twofold. Secretion of alpha MSH immunoreactivity was stimulated approximately two- and sixfold by 6.1 microM and 12.2 microM nicotine, respectively. However, nicotine (6.1 microM) had no direct effect on the secretion of beta-endorphin, alpha MSH, or ACTH immunoreactivities from the isolated superfused pituitaries. The data suggest nicotine acts in the brain to stimulate pituitary secretion of alpha MSH and beta-endorphin. Electrocorticographic (ECoG) activity of the IPMB was monitored. Nicotine induced characteristic ECoG changes including a reduction of input voltage, a biphasic response of rapid desynchronization followed by prolonged synchronization, and seizure at high doses (12.2 microM).
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PMID:Effects of nicotine on beta-endorphin, alpha MSH, and ACTH secretion by isolated perfused mouse brains and pituitary glands, in vitro. 298 5

Since ACTH and the opioids display opposite effects on experimentally-induced seizures, cerebrospinal fluid (CSF) levels of ACTH and beta-endorphin (beta-EP) were measured in 6 children (4-8 months) affected by infantile spasms with hypsarhythmia, an idiopathic early onset encephalopathy, and in 8 age-matched controls. beta-EP levels in the patients (76.3 +/- 14.7 fmol/ml, M +/- SD) did not differ from those in controls (109.8 +/- 42.7) while babies with epileptic encephalopathy showed reduced ACTH levels in the CSF (3.8 +/- 1.5) as compared to controls (9.0 +/- 3.7, p less than 0.01). This resulted in an increased beta-EP/ACTH ratio. Another patient previously treated with ACTH showed a normal CSF level of ACTH (9.0) with a normal beta-EP/ACTH ratio while in clinical and EEG remission. These results are consistent with the hypothesis that some infantile seizures unrelated to brain injuries could originate from an ACTH deficiency at central level and/or an imbalance of neuropeptidergic pathways.
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PMID:Reduced ACTH, while normal beta-endorphin CSF levels in early epileptic encephalopathies. 298 81

Adrenocorticotropic hormone (ACTH) has been frequently used as an anticonvulsant drug in some childhood seizure disorders. Despite its widespread use, few studies have evaluated the effects of ACTH on seizure susceptibility in the developing animal or the long-term consequences of ACTH treatment on brain development. In this study, ACTH was given either for 2 days or 14 days prior to kindling in 15-, 22-, and 30-day-old rats. Morphological changes in the brain were studied using routine light microscopy and dendrite branch counting following Golgi staining. Both acute and chronic ACTH treatment inhibited the rate of kindling in all three age groups. There were no differences in brain morphology between the controls and the ACTH-treated rats killed shortly after kindling. Rats treated with ACTH and killed as adults, however, had significantly more dendrite branches than did controls. In the immature brain, ACTH treatment reduces seizure susceptibility and has no long-term deleterious effects on neuronal growth.
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PMID:Effects of ACTH on seizure susceptibility in the developing brain. 301 86

There are four lines of evidence for or against a role of neuropeptides in epilepsy: Administration of a variety of opiate agonists into the ventricles or brain of animals produces a constellation of electrical and behavioral changes, seemingly receptor-specific, both sensitive to the specific opiate antagonist naloxone as well as certain anticonvulsant drugs. The primary reservation concerning these data in terms of their relevance to epilepsy regards the fact that the peptides are exogenously administered in relatively high doses. Hence, these data may reflect neurotoxic effects of peptides rather than physiologic function. A variety of opiate agonists are anticonvulsant and naloxone shortens the postictal state in some experimental seizure models. One could attempt to reconcile these data with those in No. 1 by hypothesizing that the spikes and behavioral changes examined in the latter experimental parodynes represented a sort of isolated model of the postictal state. Naloxone has little effect in clinical epilepsy. These data are far from conclusive for two reasons. First, few patients have been studied. Second, because of the issue of opiate receptor heterogeneity and the high doses of naloxone needed experimentally to block non-mu opiate effects, the doses of naloxone used clinically to date are too low to rule out possible delta- or epsilon-mediated effects. The negative clinical data are illustrative of the dangers and difficulties of extrapolating data generated in animal models of seizures to the human condition. ACTH, a peptide that is derived from the same precursor molecule as beta-endorphin, is clearly an effective anticonvulsant in certain childhood seizure states. However, whether this is due to a direct or indirect (that is, cortisol) effect on brain is far from clear. Paradoxically, in contradistinction to other data concerning pro- and anticonvulsant properties of various opioid peptides, there is no animal model of infantile spasms to help resolve this important question.
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PMID:Neuropeptides and seizures. 302 83

Very small amounts of pituitary hormones and their peptide fragments can profoundly affect learning, memory and other behaviors in both rodents and humans. In addition, several potent pituitary hormone analogs have been developed (e.g. ORG-2766) which retain the behavioral but not the endocrine properties of the parent hormone. The abilities of these peptides to influence nervous system functions suggested that they also may be capable of modifying seizure activity. This possibility is supported by the fact that treatment with adrenocorticotropic hormone (ACTH) represents a major effective therapy for at least one clinical convulsive disorder, infantile spasm. This contention also is reinforced by our findings that ORG-2766 markedly reduces both the behavioral severity and the spread of seizure potentials in an animal model of epilepsy, the kindled rat. By contrast, arginine vasopressin and its non-endocrine desglycyl fragment (DGAVP) facilitates the seizure process in this animal model. Our research also suggests that the behavioral and physiological effects of certain anterior and posterior pituitary hormone fragments depend, in part, on their abilities to modulate permeability mechanisms in brain vasculature. In addition, and especially significant from the standpoint of etiology, is the observation that the kindling process itself appears to alter cerebrovascular permeability. In the kindled rat, "permanent" decreases in permeability (60-75%) are found selectively in the hypothalamic and hippocampal regions, weeks after the last seizure. Several lines of evidence indicate that disruption of normal cerebrovascular function occurs following epileptiform seizures. We propose that an immediate increase in cerebral blood flow and cerebrovascular permeability occurs following a single, acute seizure, and that repeated chronic seizures lead to damage to the cerebrovascular system. Sustained damage would be expected to contribute to the development and maintenance of a chronic seizure focus. Such observations suggest a link between important cerebrovascular disturbances associated with seizures and the existing known and proposed electrophysiological, metabolic and neuropathological substrates of epilepsy. They also point to new strategies for the treatment of seizure disorders by focusing on ways to reduce or prevent cerebrovascular damage.
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PMID:ACTH-related peptides, kindling and seizure disorders. 303 92

Suppression of an adrenocorticotropic hormone (ACTH) response to insulin hypoglycemia has been reported in ACTH-treated adults. There are no guidelines for withdrawal of ACTH treatment in children. After observing suppressed morning cortisol in several children, insulin tolerance tests were performed in five children within 48 hours after tapered withdrawal of ACTH treatment for myoclonic seizures. ACTH response, as determined by cortisol and beta-endorphin radioimmunoassay, was adequate in four of the children. One child showed low basal levels and minimal elevation during hypoglycemia for both beta-endorphin (0 to 3 pg/ml) and cortisol (3.6 to 4.4 micrograms/dL) on initial testing, but normal responses six weeks later. Measurement of beta-endorphin response supported a central basis for suppression in the child, who had had an adrenal hemorrhage during gram-negative sepsis while on ACTH. ACTH release is transiently suppressed in some children after exogenous ACTH treatment. Tapered withdrawal and stress coverage is recommended.
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PMID:Suppressed pituitary ACTH response after ACTH treatment of infantile spasms. 303 33

An infant with congenital cytomegalovirus infection first developed seizures at six weeks of age. At 3 1/2 months of age, he developed continuous infantile spasms that lasted for more than an hour. This episode of status epilepticus was terminated by intravenous lorazepam and paraldehyde, and seizures were subsequently controlled for seven months by adrenocorticotropic hormone (ACTH), valproic acid, and phenobarbital. This case demonstrates that continuous infantile spasms may occur as a unique form of status epilepticus in young infants.
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PMID:Continuous infantile spasms as a form of status epilepticus. 303 34


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