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)

Experiments have been performed in order to evaluate the respiratory consequences of a suppression or accumulation of endogenous opioid peptides, in the neuronal network which generates the motor respiratory activity. Iontophoretic application of naloxone onto respiratory neurons increases their firing activity and increases their respiratory modulation. On the other hand the local injection of kelatorphan (an enkephalinase inhibitor) decreases the firing of respiratory neurons and thus reduces the respiratory modulation. This effect of kelatorphan mimics the effect on respiratory neuron of an iontophoretic application of met-enkephalin. Furthermore the local injection of kelatorphan reduces the frequency of the respiratory output recorded from the phrenic nerve. This effect is reversed by systemic administration of naloxone. The results demonstrate the involvement of endogenous opioid peptides in the control of breathing suggesting that in Sudden Infant Death Syndrome a possible dysregulation in opioidergic system could occur.
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PMID:Control of breathing by endogenous opioid peptides: possible involvement in sudden infant death syndrome. 130 13

Beta-endorphin (BE) and neurotensin (NT) are two neuropeptides which induce apneas. In infants who died of Sudden Infant Death Syndrome (SIDS) we measured, in brainstem and CSF, BE and NT by IRMA and RIA respectively. BE and NT levels are compared to same aged infant and adult controls. CSF BE level was significantly higher in SIDS than in the two control groups (86 +/- 14 vs 33 +/- 13 and 16 +/- 5 pmol/l). In 6 SIDS victims NT and BE were assayed in 5 brainstem sections, each of them divided in median, intermediate and lateral parts. We found high levels of BE in every fragment (3-11 pmol/mg protein) while NT elevated values were restricted to the mesencephalic regions (1.4-12 pmol/mg), the medial pons (6 pmol/mg) and the intermediate parts of the medulla (including the olive: 1.3-1.6 pmol/mg). These results support the hypothesis that NT and/or BE could induce or participate to the fetal issue of SIDS.
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PMID:Beta-endorphin and neurotensin in brainstem and cerebrospinal fluid in the sudden infant death syndrome. 130 24

To gain further insight into the possible role of endogenous opioid peptides in the respiratory difficulties associated with the apnea of infancy and other disorders possibly related to apnea, the levels of beta-endorphin immunoreactivity were measured in the cerebrospinal fluid (CSF) of five groups of infants: (1) infants with proved apnea, (2) infants with histories of an apparent life-threatening event (ALTE), (3) siblings of victims of the sudden infant death syndrome (SIDS), (4) infants with suspected but unproved apnea, and (5) infants undergoing investigation for other acute illnesses. Twenty-two infants considered at risk for an ALTE (groups 1 to 3) had significantly higher CSF beta-endorphin equivalents (88 +/- 7 pg/mL) than did the 22 control patients in groups 4 and 5 (31 +/- 3 pg/mL). Plasma beta-endorphin immunoreactivity, which was also measured in some of the infants, did not correlate with levels in CSF and, in fact, was significantly lower in the groups at risk for an ALTE (50 +/- 9 pg/mL; n = 14) than in the control subjects (80 +/- 6 pg/mL; n = 11). These studies indicate that elevated beta-endorphin immunoreactivity in CSF may be a marker in infants who have apnea and who may be considered at risk for an ALTE.
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PMID:Increased cerebrospinal fluid beta-endorphin immunoreactivity in infants with apnea and in siblings of victims of sudden infant death syndrome. 295 62

Immunohistochemical localization of beta-endorphin was studied in the pituitaries and medullas of forty human infants at autopsy. beta-Endorphin immunoreactivity was found in anterior pituitary cells in all cases. In the medulla, beta-endorphin immunoreactivity was found in the neurons of the medial and lateral cuneate nuclei in ten out of the forty cases. In eight of these ten cases, the infants died of causes other than sudden infant death syndrome (SIDS). Only two of 25 SIDS cases had demonstrable beta-endorphin in the brainstem nuclei. Beta-endorphin levels in the spinal fluids of all the cases showed no correlation to cause of death, age or gender.
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PMID:Beta-endorphin in the brainstem, pituitary, and spinal fluid of infants at autopsy: relation to sudden infant death syndrome. 297 25

To investigate the possible role of the endogenous opioid system in the pathogenesis of the sudden infant death syndrome (SIDS), we measured met-enkephalin immunoreactivity by radioimmunoassay in brain, lung, and adrenal glands of SIDS victims and of infants (controls) dying of nonneurologic causes. Met-enkephalin was stable in brain tissue up to 24 hours after death. On inspection, met-enkephalin levels in the cerebral cortex of SIDS victims were similar to those in controls. Levels in the caudate nucleus were lower in infants than in adults. In the medulla, the levels in SIDS cases and controls were not found to differ significantly. The linear relationship between the levels in the medulla and age was not detectably different in SIDS and controls. However, as a subset, levels in the control group significantly decreased with increasing age (P = 0.005), whereas levels in the SIDS group showed no correlation with age (P = 0.33). Levels of met-enkephalin in the adrenal gland of SIDS victims were similar to those in controls and were considerably lower than adult values. Lung tissue was assayed for beta-endorphin immunoreactivity and met-enkephalin: for both peptides the values in SIDS cases were low (femtomolar range) and similar to those in controls. These data suggest that met-enkephalin is not markedly overproduced in brains of SIDS victims. Future postmortem studies should focus on more subtle evidence of endogenous opioid overactivity such as differences in age related changes, receptor number, and levels of other endogenous opioid peptides.
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PMID:A study of the endogenous opioid system in the sudden infant death syndrome. 630 2

Double-label immunocytochemistry was used to investigate the colocalisation of various neuropeptides and the enzymes nitric oxide synthase (NOS) and tyrosine hydroxylase (TH) in intramural ganglia of the human male urinary bladder neck and trigone. Postmortem specimens were obtained from 7 male infants and children ranging in age from 2 mo to 3 y who had died as a result of cot death or accidental trauma. On average 60% of the intramural neurons were non-TH-immunoreactive (-IR) (i.e. presumptive cholinergic) and 40% were TH- and D beta H-IR (i.e. noradrenergic). Within the non-TH-IR population, calcitonin gene-related peptide (CGRP) was found in 65% of cells, neuropeptide Y (NPY) in 90%, nitric oxide synthase (NOS) in 45%, somatostatin (SOM) in 90%, and vasoactive intestinal polypeptide (VIP) in 40%. The corresponding values for the TH-IR neurons were CGRP (54%), NPY (70%), NOS (58%), SOM (73%) and VIP (40%). All the observed bombesin (BOM)-immunoreactivity was colocalised with TH while 90% of VIP and almost all the CGRP was colocalised with NPY. Less than 5% of neurons were immunoreactive for substance P (SP) or met-enkephalin (m-ENK) and some of these also contained TH. Varicose nerve fibres were seen in close proximity to some of the intramural neurons, the majority of such varicosities showing immunoreactivity to CGRP, VIP or TH. Less common were pericellular varicosities immunoreactive to NPY, SOM or SP. These results demonstrate the neurochemical heterogeneity of intramural neurons in the human bladder neck and provide indirect evidence for the complexity of the peripheral innervation of the human urinary bladder.
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PMID:A double-label immunohistochemical study of intramural ganglia from the human male urinary bladder neck. 903 88

The effects of prenatal exposure to carbon monoxide (CO), a major component of cigarette smoke, was studied alone or in combination with postnatal hyperthermia, on the structural and neurochemical development of the postnatal brain at 1 and 8 weeks. Pregnant guinea pigs (n = 11) were exposed to 200 p.p.m CO for 10 h/day from midgestation until term (68 days), whereas control mothers (n = 10) breathed room air. On postnatal day 4, neonates from the control and CO-exposed pregnancies were exposed to hyperthermia (35 degrees C) for 75 min or remained at ambient (23 degrees C) temperature. Using semiquantitative immunohistochemical techniques the following neurotransmitter alterations were found in the medulla at 1 week: a decrease in met-enkephalin-immunoreactivity (IR) following postnatal hyperthermia and an increase in 5-hydroxytryptamine-IR following a combination of CO and hyperthermia. No alterations were observed in substance P- or tyrosine-hydroxylase-IR in any paradigm. At 8 weeks of age the combination of prenatal CO exposure followed by a brief hyperthermic stress postnatally resulted in lesions throughout the brain and an increase in glial fibrillary acidic protein-IR in the medulla. Such effects on brain development could be of relevance in cardiorespiratory control in the neonate and could have implications for the etiology of Sudden Infant Death Syndrome, where smoking and hyperthermia are major risk factors.
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PMID:Exposure to prenatal carbon monoxide and postnatal hyperthermia: short and long-term effects on neurochemicals and neuroglia in the developing brain. 1073 30

Maternal cigarette smoking during pregnancy is associated with a significantly increased risk of Sudden Infant Death Syndrome (SIDS). This study investigated the effects of prenatal exposure to carbon monoxide (CO), a major component of cigarette smoke, on the neuroglial and neurochemical development of the medulla in the fetal guinea pig. Pregnant guinea pigs were exposed to 200 p.p.m CO for 10 h per day from day 23-25 of gestation (term = 68 days) until day 61-63, at which time fetuses were removed and brains collected for analysis. Using immunohistochemistry and quantitative image analysis, examination of the medulla of CO-exposed fetuses revealed a significant decrease in tyrosine hydroxylase-immunoreactivity (TH-IR) in the nucleus tractus solitarius, dorsal motor nucleus of the vagus (DMV), area postrema, intermediate reticular nucleus, and the ventrolateral medulla (VLM), and a significant increase in choline acetyltransferase-immunoreactivity (ChAT-IR) in the DMV and hypoglossal nucleus compared with controls. There was no difference between groups in immunoreactivity for the m2 muscarinic acetylcholine receptor, substance P- or met-enkephalin in any of the medullary nuclei examined, nor was there evidence of reactive astrogliosis. The results show that prenatal exposure to CO affects cholinergic and catecholaminergic pathways in the medulla of the guinea pig fetus, particularly in cardiorespiratory centers, regions thought to be compromised in SIDS.
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PMID:Chronic prenatal exposure to carbon monoxide results in a reduction in tyrosine hydroxylase-immunoreactivity and an increase in choline acetyltransferase-immunoreactivity in the fetal medulla: implications for Sudden Infant Death Syndrome. 1074 60