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)

We report four patients with infantile spasms and the congenital bilateral perisylvian syndrome. Onset of spasms occurred during the first 6 months of life. Response to corticotropin treatment was prompt and resulted in resolution of seizures in all patients. Epilepsy developed in the four children after an interval of 2 to 12 years. Developmental outcome was variable; three were severely restricted and one was married and lived independently. Imaging studies revealed bilateral perisylvian lesions characteristic of polymicrogyria. Infantile spasms may be the presenting seizure type in some patients with the congenital bilateral perisylvian syndrome.
 ...
PMID:Infantile spasms: an early epileptic manifestation in some patients with the congenital bilateral perisylvian syndrome. 782 36

1. The effects of corticotropin-releasing hormone (CRH) on synaptically evoked population and intracellular responses in the isolated rat CA1 region of hippocampal slices were studied to evaluate possible differences between adult and juvenile rats. 2. The amplitude of orthodromically evoked (stratum radiatum stimulation) population spikes was reversibly enhanced by 0.2-0.6 microM CRH to a greater extent in slices from juvenile rats than from adult rats. In no case, however, did CRH cause seizure-like activity to develop under normal recording conditions. 3. In the presence of 10-30 microM bicuculline, interictal-like bursts of population spikes and corresponding intracellularly recorded action potentials could be evoked starting at postnatal day 8. The number of spikes and the duration of the evoked bursts in the CA1 region were reversibly increased by CRH (0.2-0.6 microM) to a greater extent in slices from juvenile than from adult rats. 4. The amplitude of the afterhyperpolarization following intracellularly evoked bursts of action potentials in CA1 pyramidal cells was reduced by 0.2 microM CRH to a similar degree in both young and adult rats. No consistent changes in input resistance or membrane potential were observed. 5. No correlation was found between the magnitude of the CRH-induced increase in responsiveness and the initial excitability in controls, suggesting that the CRH-induced changes were independent of any age-dependent differences in general slice excitability. 6. Our results indicate that, in the CA1 region, CRH augments bicuculline-induced bursts to a greater extent in slices from young versus adult rats.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Age-related epileptogenic effects of corticotropin-releasing hormone in the isolated CA1 region of rat hippocampal slices. 788 62

We examined whether glucocorticoids could enhance the ability of corticotropin-releasing hormone (CRH) to induce seizures. Rats were treated with systemic glucocorticoids (dexamethasone, 100 micrograms) or vehicle for either 3 days (chronic) or 2 h (acute) before intracerebroventricular CRH (3 or 10 micrograms) or saline injections and then monitored for 8 h following each injection. Our results suggest that chronic, but not acute, glucocorticoid pretreatment increases the likelihood of CRH-induced seizures.
 ...
PMID:Glucocorticoid treatment increases the ability of CRH to induce seizures. 797 Jan 44

We measured lumbar cerebrospinal fluid (CSF) levels of somatostatin, cholecystokinin, neurotensin, atrial natriuretic factor, vasoactive inhibitory peptide, neuropeptide Y, adrenocorticotrophic hormone, corticotropin releasing hormone, beta-endorphin, metenkephalin, cortisol, alanine, glycine, aspartate, glutamate, taurine, and gamma-aminobutyric acid in 25 inpatients with epilepsy at known interictal and postictal times and in 11 neurologically normal volunteers. There were no significant differences between interictal or postictal complex partial seizures (CPS), postictal generalized tonic-clonic seizures (GTC), and control CSF neuropeptide, cortisol, and amino acid (AA) levels. However, there were nonsignificant trends for CSF levels of several neuropeptides to be increased after CPS and GTC as compared with interictal baseline levels. There were significant correlations between levels of certain CSF neuropeptides or (AAs) and serum antiepileptic drug (AED) levels. Several correlations were noted between CSF levels of AAs, including a correlation between the excitatory neurotransmitters aspartate and glutamate identified only after CPS.
 ...
PMID:Cerebrospinal fluid levels of neuropeptides, cortisol, and amino acids in patients with epilepsy. 809 91

The effects of some beta-endorphin fragments with neuroleptic-like properties, i.e., tau-endorphin, des-tyr1-tau-endorphin (DT tau E), desenkephalin-tau-endorphin (DE tau E), in comparison with the dopaminergic antagonist haloperidol,- were studied on the EEG and behavioral alterations induced by beta-endorphin in the rabbit. beta-Endorphin administered i.c.v. (5-30 nmol) induced EEG nonconvulsive limbic seizures as well as EEG background and behavioral alterations which were antagonized by naloxone administered i.v. (1-2 mg/kg). Haloperidol, tau-endorphin, DT tau E and DE tau E were unable to prevent beta-endorphin-induced alterations when injected in a single dose i.v. (25-50 micrograms/kg), 15 min before beta-endorphin. Subchronic i.v. administration of DT tau E or DE tau E (25 micrograms/kg/day) for 4 consecutive days prevented completely EEG limbic seizures as well as EEG background and behavioral alterations induced by i.c.v. beta-endorphin injected 15 min after the fourth dose; however, haloperidol (30 micrograms/kg/day) administered with the same schedule as DT tau E or DE tau E was able to prevent only EEG epileptiform and EEG background alterations induced by beta-endorphin. tau-Endorphin administered i.v. for 4 consecutive days (25 micrograms/kg/day) did not consistently influence any of the beta-endorphin effects. Our results show that DT tau E and DE tau E, which are devoid of opioid activity, exert a strong antagonism on ictal seizures as well as on other EEG alterations and behavioral alterations induced by beta-endorphin, and suggest that the antagonism shown by these drugs and by haloperidol on the EEG effects induced by beta-endorphin are exerted at least in part through an indirect action, i.e., an interaction with the dopaminergic system.
 ...
PMID:Subchronic treatment with fragments of beta-endorphin prevents electroencephalographic seizures and behavioral alterations induced by centrally administered beta-endorphin in the rabbit. 811 60

We report that glucocorticoids significantly facilitated the development of cocaine-induced kindled seizures. These results suggest that glucocorticoids may have effects on the development of kindled seizures which are similar to those of the neuropeptide, corticotropin-releasing hormone (CRH), with which they show a close functional relationship. These results may be of interest in the light of data showing that glucocorticoids increase CRH expression in the central nucleus of the amygdala, which is an important site for the development of kindling.
 ...
PMID:Facilitation of cocaine kindling by glucocorticoids in rats. 828 72

A number of stimuli including acute footshock and electrically-induced seizures lead to release of beta-endorphin immunoreactivity from the anterior pituitary corticotropes. Gel filtration of this beta-endorphin immunoreactivity indicates that approximately 3-fold more beta-endorphin than beta-lipotropin is released into plasma following these acute stressors. A similar preponderance of beta-endorphin over beta-lipotropin is seen in the media of short-term anterior lobe cell suspensions stimulated with ovine corticotropin-releasing hormone. Previous studies indicated that footshock stress, when administered repeatedly, can increase the biosynthesis of anterior lobe proopiomelanocortin (POMC) as indicated by increased steady state adrenocorticotropin/beta-endorphin content as well as increased POMC mRNA levels and increased POMC biosynthesis and rate of processing as measured by pulse-labeling and pulse-chase studies. The goal of the present studies was to determine whether this increased biosynthetic drive results in an alteration in the end products secreted with repeated stress. Acute footshock in a rat which has received 14 days of chronic footshock releases proportionately more beta-lipotropin than is released in a naive rat. Chronic electrically-induced seizures, which also increase anterior lobe POMC derived peptide stores, lead to a similar shift in the ratio of beta-lipotropin:beta-endorphin released following stress. These data suggest that chronic drive and the subsequent changes in POMC peptide stores may lead to a decrease in the proportion of beta-endorphin size immunoreactivity in the releasable pool of the anterior lobe corticotrope, thus altering the hormonal signal from the anterior lobe corticotrope.
 ...
PMID:Altered ratios of beta-endorphin:beta-lipotropin released from anterior lobe corticotropes with increased secretory drive. II. Repeated stress. 838 74

Massive infantile spasms are an age-specific seizure syndrome of infancy. Uniquely, the spasms respond to hormonal manipulation using adrenocorticotropic hormone (ACTH) or glucocorticoids. A hypothesis explaining the efficacy of hormonal therapy, age-specificity, multiple causative factors, and spontaneous resolution of infantile spasms is presented. Corticotropin-releasing hormone (CRH), an excitant neuropeptide suppressed by ACTH/steroids, is implicated. Evidence for the age-specific convulsant properties of CRH is presented, and a putative scenario in which a stress-induced enhancement of endogenous CRH-mediated seizures is discussed. Clinical testing of the CRH-excess theory and its therapeutic implications are suggested.
 ...
PMID:Pathophysiology of massive infantile spasms: perspective on the putative role of the brain adrenal axis. 838 75

We report 16 patients with infantile spasms in whom onset of the clusters of spasms appeared to be triggered by close temporal association with partial seizures. Common features included the presence of focal cerebral lesions in 12 infants (3 were classifiable as cryptogenic); all had partial seizures with EEG localization, clusters of bilateral spasms always preceded by partial seizures, and response to adrenocorticotropic hormone (ACTH) and traditional antiepileptic drugs (AEDs) generally was poor. Three had complete agenesis of the corpus callosum, which argues against interhemispheric callosal spread of focal discharges resulting in the generalized spasms. Surgical cortical resections were performed in 6 of the infants, with good outcomes. This group of patients supports a model in which the spasms, although probably generated at a subcortical level, are facilitated or possibly induced by focal discharges from cortical pathology.
 ...
PMID:Facilitation of infantile spasms by partial seizures. 842 69

Circadian effects on PTZ-induced seizure thresholds alone and following drug pretreatment were studied in 720 male rats, divided into 40 groups of 18 each. Each rat was tested only once, at one of eight clock hours and under one of five drug pretreatments. Clear cyclic changes in thresholds were found. Drug effects on the rhythm were similar for DSIP and beta-endorphin, which produced higher thresholds during the night periods, while d-amphetamine and melatonin decreased the threshold during that period. All drugs increased the vulnerability to seizures relative to the saline control during the daytime, while only beta-endorphin and DSIP offered improved protection during the night hours. The possibility of dopaminergic mediation is suggested to account for the effects.
 ...
PMID:Circadian effects of beta-endorphin, melatonin, DSIP, and amphetamine on pentylenetetrazol-induced seizures. 848 98


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