Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whole-cell patch-clamp recordings were used to investigate nicotinic acetylcholine receptors (nAChRs) in the human neuroblastoma cell line, SH-SY5Y. Acetylcholine, nicotine and the neuronal nAChR agonist dimethylphenylpiperazinium iodide (DMPP), but not muscarine, all evoked inward currents in the cells (voltage-clamped at -60 mV). DMPP's actions were concentration- and voltage-dependent, and were antagonised by the neuronal nAChR antagonist mecamylamine (1-3 microM). Atropine was ineffective at 0.1 microM, but at 1 microM caused significant reductions in current amplitudes. Pre-incubation of cells with 2 microM alpha-cobratoxin had no effect on the actions of DMPP, and inward currents could also be induced when extracellular NaCl was replaced with CaCl2. DMPP also reversibly depolarized SH-SY5Y cells. These findings clearly identify nAChRs in SH-SY5Y cells, and provide two possible mechanisms by which receptor activation may lead to noradrenaline release, namely by triggering Ca2+ influx through the nAChR itself or by opening voltage-gated Ca2+ channels.
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PMID:Nicotinic acetylcholine receptors in human neuroblastoma (SH-SY5Y) cells. 146 17

The relationship between 6-hydroxydopamine (6-OHDA)-induced ablation of central and peripheral adrenergic neurons and in situ C-1300 murine neuroblastoma (MNB) tumor growth and catecholamine concentration were investigated. Destruction of central and/or peripheral adrenergic neurons was produced by the intracerebral and/or s.c. administration of 6-OHDA to neonatal A/J mice. Disaggregated MNB cells (1 x 10(6)) were implanted s.c. into each mouse 3 weeks after treatment with 6-OHDA or diluent. Tumor onset time (the time interval between implantation of MNB cells and detection of palpable tumor), tumor weight, tumor weight to body weight ratio, tumor growth rate constant and tissue catecholamine concentrations were determined. Central axotomy caused a significant increase in tumor onset time and decrease in tumor weight when compared to controls. However, neither the tumor weight to body weight ratio or tumor growth rate constant were significantly lowered. In contrast, a reduction in all tumor growth parameters was produced by peripheral axotomy, which differed significantly from centrally axotomized and control animals. The catecholamine concentration of MNB tumors excised from control and 6-OHDA-treated mice 8 days after tumor onset were determined. Norepinephrine and dopamine levels were elevated above controls in MNB tumors obtained from mice that had been either peripherally or peripherally and centrally axotomized; whereas, no change in tumor catecholamine concentrations was noted in centrally axotomized mice. This investigation has demonstrated that ablation of central as well as peripheral adrenergic innervation exerts an inhibitory effect on MNB tumor growth.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of 6-hydroxydopamine-induced ablation of peripheral and central adrenergic axons on C-1300 murine neuroblastoma tumor growth and catecholamine concentration in the A/J mouse. 152 14

The authors report the case of a tetralogy of Fallot associated with a neuroblastoma secreting large quantities of noradrenaline. Anoxic decompensation of the tetralogy of Fallot occurred early at the age of 4 months with cyanotic crises associated with an impression of abdominal pain. A systemic-pulmonary anastomosis was performed and the cyanosis regressed but the crises persisted and investigations showed the presence of a neuroblastoma. The tumour was treated by surgery and chemotherapy and has not recurred after 2 years' follow-up. Complete repair of the tetralogy of Fallot was performed secondarily at the age of 2. In this case, the high concentration of circulating catecholamines was probably a factor of early decompensation of the tetralogy of Fallot by infundibular spasm. A review of the literature revealed 26 cases of cardiac disease with a peripheral neurogenic tumour. Two pathogenic mechanisms are suggested: an embryological abnormality of cardiac cell migration from the neural crest and chronic stimulation of neuroblastic cells by chronic hypoxia.
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PMID:[Neuroblastoma, factor of early decompensation of tetralogy of Fallot]. 153 Apr 3

The human SH-SY5Y neuroblastoma cell line displays morphological, neurochemical, and electrophysiological characteristics of sympathetic neurons. mu-Opioid receptors mediate inhibition of the N-type calcium current present in these cells. Here we have studied the effects of chronic incubation with morphine (1 microM for 3-7 days) in vitro on the inhibition of this current induced by mu-opioid agonists and noradrenaline. In untreated control cells the mu-opioid agonists and noradrenaline. In untreated control cells the mu-opioid agonists morphine (1 microM) and [D-Ala2,N-MePhe4,Gly-ol] enkephalin (DAMGO) (10 nM to 1 microM), and noradrenaline (10 nM to 10 microM) inhibited the calcium current to a similar extent. The maximal effects of DAMGO and noradrenaline were not additive. Chronic exposure to morphine had no effect on the maximum amplitude of the calcium current evoked or on its voltage sensitivity. However, the concentration-response curve to DAMGO was shifted to the right in a parallel manner, with a 7-fold increase in the IC50 value but no change in the maximum inhibition produced. In contrast, the maximum inhibition in response to morphine appeared to be substantially reduced. Noradrenaline inhibited the calcium current equally in untreated and morphine-tolerant cells. Thus, it is concluded that morphine-induced tolerance to inhibition of the N-type calcium current occurs at the single-cell level and is homologous to the mu-opioid receptor. Also, morphine appears to be an agonist of lower efficacy than DAMGO. The results are consistent with tolerance being due to a functional reduction in the mu-opioid receptor reserve, probably by disruption of the receptor/GTP-binding protein interaction.
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PMID:Mu-opioid receptor inhibition of calcium current: development of homologous tolerance in single SH-SY5Y cells after chronic exposure to morphine in vitro. 166 36

The effect of calcium channel antagonists on depolarization and carbachol evoked release of [3H]noradrenaline in the human neuroblastoma, SH-SY5Y, was investigated. Nifedipine, verapamil and diltiazem completely inhibited the depolarization evoked release of [3H]noradrenaline with IC50 values of 0.44 +/- 0.1 microM, 3.6 +/- 0.24 microM and 5.6 +/- 0.2 microM respectively. In addition, nickel, cobalt and cadmium, all at 2 mM, inhibited depolarization evoked release by 89.2 +/- 2.3%, 72.6 +/- 1.6% and 102.5 +/- 1.4% respectively. Furthermore, omega-conotoxin resulted in at least 20% inhibition of potassium evoked release, suggesting a role of N-type calcium channels. Carbachol evoked release of [3H]noradrenaline was inhibited by 10(-4) M nifedipine, diltiazem and verapamil by 15.6 +/- 1.1%, 14.6 +/- 3.2% and 23.6 +/- 1.8% respectively and by 2 mM nickel, cobalt and cadmium by 13.8 +/- 3.2%, 34 +/- 2.1% and 6.5 +/- 3.7% respectively. These results suggest that depolarization evoked release of [3H]noradrenaline is mediated via L- and N-type calcium channels, whereas, carbachol evoked release does not appear to be coupled an L-, T- or N-type voltage sensitive calcium channel.
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PMID:The effect of calcium channel antagonists on the release of [3H]noradrenaline in the human neuroblastoma, SH-SY5Y. 174 5

The results of calculations of urinary dopamine/noradrenaline (DA/NAd) and dopamine/vanillylmandelic acid (DA/VMA) ratios in 54 untreated children with neuroblastic tumors are reported. Thirteen patients were in the prognostically favorable group (stages I, II, and IV-S and ganglioneuroma [GN]), and 41 had advanced neuroblastoma (stage III and IV). Among patients with ganglioneuroma and favorable neuroblastoma (n = 13), of whom all were survivors, the urinary DA/NAd and DA/VMA ratios exceeded 1.8 in only 2 cases of stage IV-S and stage I, respectively. In the advanced neuroblastoma group, the DA/NAd and DA/VMA ratios exhibited a wide range of values, but among the stage III and IV survivors (n = 10), DA/NAd ratios greater than 1.8 were noted in only 3 patients. The DA/VMA ratio was not greater than 1.8 in those 3 patients. The mean DA/NAd and DA/VMA proportions in the population comprising all survivors were 1.8 +/- 2.7 (mean +/- SD) and 1.1 +/- 0.4, respectively. The same computations carried out in patients who died showed higher values, ie, the mean DA/NAd and DA/VMA ratios were 5.2 +/- 6.3 and 5.6 +/- 10.5, respectively, showing the difference in DA/NAd and DA/VMA ratios between prognostically favorable and unfavorable groups. Of 23 survivors, only 4 had DA/NAd ratios greater than 1.8 (17%), while 24 of 31 children who died (77%) had DA/NAd ratios was greater than 1.8. The reported results suggest dissimilarity in the catecholamine metabolism of adrenergic clones with respect to the stage of advancement of neoplastic disease.
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PMID:Urinary dopamine/noradrenaline and dopamine/vanillylmandelic acid ratios as a reflection of different biology of adrenergic clones in children's neuroblastic tumors. 177 34

We report 93 patients with catecholamine producing tumors that were analyzed at the Hormone Laboratory of the Institute of Cardiology. They are 75 pheochromocytoma patients and 18 children with neuroblastoma. Fluorimetric methods were used to measure urinary and plasma catecholamines on neuroblastoma and pheochromocytoma patients. Dopamine high excretion (mean value 2889 micrograms/24 hs), was constantly observed in the neuroblastoma children as were adrenaline and noradrenaline in the benign and malignant pheochromocytoma patients. The mean values for the malignant tumours were 53 for adrenaline and 1436 micrograms/24 hs for noradrenaline. Structural and biochemical differences of the catecholamine producing tumours are reflected on the clinical manifestations which are observed in the patients bearing such neoplasms.
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PMID:[Catecholamine-producing tumors]. 179 8

The human neuroblastoma clone SH-SY5Y expresses potassium-, carbachol-, and calcium ionophore A23187-evoked, calcium-dependent release of [3H]noradrenaline. Release in response to carbachol and potassium was greater than additive. Atropine (Ki = 0.33 nM), hexahydrosiladifenidol (Ki = 18 nM), and pirenzepine (Ki = 1,183 nM) completely inhibited the carbachol-evoked noradrenaline release, an order of potency suggesting that an M3 receptor was linked to release. In contrast, noradrenaline release was only partially inhibited by the M2-selective antagonists methoctramine (10(-4) M) and AFDX-116 (10(-4) M), by approximately 14 and 46%, respectively. The nicotinic antagonist d-tubocurarine (10(-4) M) resulted in a partial inhibition of release, a finding suggesting that a nicotinic receptor may also be involved. SH-SY5Y provides a suitable cell line in which to study the biochemical mechanisms underlying the cholinergic receptor regulation of noradrenaline release.
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PMID:Potassium- and carbachol-evoked release of [3H]noradrenaline from human neuroblastoma cells, SH-SY5Y. 190 96

The effects of metoclopramide (MCP) and bromocriptine (BC) on the growth of neuroblastoma (NB) cells and their influence on the plasma membrane binding of several neurotransmitters were studied. In the first part of this study, in vitro experiments were done with three human and two murine NB cell lines. Dibutyryl cyclic 3',5'-adenosine monophosphate is known to differentiate NB cells in vitro and served as a reference substance during the experiments. MCP significantly reduced the replication rate in NB cells and increased cellular differentiation by morphological as well as by functional criteria. BC, in contrast, stimulated cell replication. Similar to dibutyryl cyclic 3',5'-adenosine monophosphate, MCP increased the binding capacity of the plasma membrane for the beta-adrenergic hormones dopamine and noradrenaline. In the second part, the effects of BC and MCP upon NB tumor growth were investigated in vivo in the mouse. Significant changes in tumor growth were induced; BC promoted and MCP inhibited the NB tumor growth in a dose-dependent relationship. The findings are discussed, along with the observed accompanying changes in serum copper and in the peripheral blood count.
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PMID:Influence of metoclopramide and bromocriptine upon the growth of human and murine neuroblastoma cells. 196 34

Regulation of the expression of procholecystokinin (proCCK) and proenkephalin A mRNA was studied in the human neuroblastoma cell line SK-N-MC. Cells were treated with dibutyryl-3',5'-cyclic AMP (dbcAMP), noradrenaline or isoproterenol, a beta-adrenoceptor agonist. Levels of proCCK and proenkephalin A mRNA were determined by Northern blot analysis with proCCK- and proenkephalin A-specific cRNA hybridization probes 9 h after drug treatments. ProCCK and proenkephalin A mRNA were co-expressed in SK-N-MC cells. ProCCK mRNA levels were increased 1.5-2.5 times by dbcAMP, noradrenaline and isoproterenol when compared with controls. The level of proenkephalin A mRNA increased approximately two to three times under the same drug conditions, whereas the level of N-myc mRNA did not change significantly. These results suggest that expression of proCCK and proenkephalin A mRNA may be regulated by a similar cAMP-dependent mechanism in the SK-N-MC cell line.
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PMID:Procholecystokinin and proenkephalin A mRNA expression is modulated by cyclic AMP and noradrenaline. 215 52


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