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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of chronic membrane depolarization on the regulation of muscarinic acetylcholine receptor (mAChR) number was studied in neuroblastoma cells (clone N1E-115). Receptor number was determined by a filter binding assay using 3H-quinuclidinyl benzilate (QNB) in membrane and crude cellular homogenates. Incubation with 50 microM veratridine (VTN), an activator of voltage-sensitive Na+ channels, induced a 50-200% increase in mAChR number at 24 hr, which was inhibited 80% by TTX. Scatchard analysis showed that affinity of the mAChR for 3H-QNB was not affected by VTN. Upon withdrawal of VTN, mAChR number returned to control levels within 20 hr. Chronic membrane depolarization caused by incubation in medium containing 60 mM K+ induced a TTX-insensitive 50% increase in mAChR number at 24 hr. AChE activity was unaffected by chronic membrane depolarization. The VTN-induced increase in mAChR number was not blocked by coincubation with cycloheximide or tunicamycin, both inhibitors of de novo mAChR synthesis. The rate of mAChR degradation was reduced in the presence of 50 microM VTN, with the apparent half-life increased from approximately 18 hr (control) to approximately 40 hr (VTN). Although treatment with either 1 mM 8Br-cAMP or 1 mM 8Br-GMP failed to increase mAChR number, treatment with either the inorganic Ca2+ channel blocker Co2+ (1 mM) or the organic Ca2+ channel antagonist D600 (10-100 microM) produced 40-80% increases in mAChR number. The combination of VTN and either D600 or Co2+ failed to induce a greater increase in mAChR number than incubation with VTN alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of muscarinic acetylcholine receptor number in cultured neuronal cells by chronic membrane depolarization. 303 81

1. The role of inositol 1,4,5-trisphosphate (InsP3) and diacylglycerol (DAG) as possible mediators of the membrane current responses of NG108-15 neuroblastoma x glioma hybrid cells to bradykinin (BK, Brown & Higashida, 1988b) has been tested using intracellular ionophoresis of InsP3 and external application of phorbol dibutyrate (PDBu) and 1-oleoyl-2-acetylglycerol (OAG). 2. Intracellular ionophoresis of InsP3 into cells clamped at -30 to -50 mV produced (i) a transient outward current, (ii) a transient outward current followed by an inward current, or (iii) an inward current. All currents were accompanied by an increased input conductance. 3. The transient outward current reversed at between -80 and -90 mV. The reversal potential was shifted to more positive potentials on raising extracellular [K+], suggesting that it resulted from an increased K+ conductance. 4. The outward current was inhibited by apamin (0.4 microM) or d-tubocurarine (0.2-0.5 mM); these drugs also inhibit the outward current produced by BK or by intracellular Ca2+ injections (Brown & Higashida, 1988 a, b). The outward current was also slowly reduced in 0 mM [Ca2+] or 0.5 mM [Cd2+] plus 2 mM [Co2+] solution. 5. Ionophoretic injection of inositol 1,3,4-trisphosphate and inositol 1,3,4,5-tetrakisphosphate, guanosine trisphosphate or inorganic phosphate did not evoke an outward current but produced only an inward current with an increased conductance, reversing at between -10 and -20 mV. 6. Bath application of PDBu (10 nM-1 microM) or OAG (1-10 microM) produced an inward current with a fall in input conductance. The inward current was voltage dependent and was accompanied by an inhibition of the time-dependent current relaxations associated with activation or deactivation of the voltage-dependent K+ current, IM. 7. PDBu did not clearly reduce the Ca2+ current or the Ca2+-dependent K+ current recorded in these cells. During superfusion with PDBu, the outward current produced by intracellular ionophoresis of InsP3 was greatly enhanced. 8. The results support the view that the two membrane current responses to BK might both result from accelerated membrane phosphatidylinositide hydrolysis. One product, InsP3, releases Ca2+ and activates an apamin-curare-sensitive outward K+ current; this effect is imitated by intracellular InsP3 ionophoresis. The second product, DAG; activates protein kinase C to inhibit the voltage-dependent K+ current IM and generate an inward current; this effect is imitated by external application of PDBu or OAG.
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PMID:Inositol 1,4,5-trisphosphate and diacylglycerol mimic bradykinin effects on mouse neuroblastoma x rat glioma hybrid cells. 326 93

Primary neuroblastoma of the kidney in adults is an extremely rare neoplasm that had not been described in the literature until 1986. The diagnosis can be made by histopathological examination only. We report 2 unusual cases of neuroblastoma of the kidney in adults. In both patients right nephrectomy was performed after the diagnosis of right renal cell carcinoma was made. Histological examination revealed the tumors to be primary neuroblastomas of the right kidney. In the first patient cobalt therapy was administered to the tumor bed and para-aortic area. Followup at 5 years revealed no sign of tumor recurrence. Progressive disseminated disease has been documented in the second patient despite postoperative adjuvant chemotherapy with combined cis-platinum and epipodophyllotoxin, and combined vincristine, cyclophosphamide, doxorubicin and dimethyl-tri-azeno imidazole carboxamine.
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PMID:Two cases of primary neuroblastoma of the kidney in adults. 357 99

A method is described for the determination of cobalt in foods. After wet digestion, iron in the sample is removed by liquid-liquid extraction, and cobalt is isolated and extracted. Final determination is done by flame atomic absorption spectrophotometry. Analysis of NBS reference materials by this procedure gives results in close agreement with certified values. The limit of quantitation is 4.3 ng/mL. Recovery studies and analysis of standard materials show that this method is reliable.
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PMID:Atomic absorption spectrophotometric determination of cobalt in foods. 401 77

The voltage-dependent Na+ ionophore of various neuronal cells is permeable not only to Na+ ions but also to guanidinium ions. Therefore, the veratridine- (or aconitine-)stimulated influx of [14C]guanidinium in neuroblastoma x glioma hybrid cells was measured to characterize the Na+ ionophore of these cells. Half-maximal stimulation of guanidinium uptake was seen at 30 microM veratridine. At 1 mM guanidinium, the veratridine-stimulated uptake of guanidinium was lowered to 50% by approximately 60 mM Li+, Na+, or K+ and by a few millimolar Mn2+, Co2+, or Ni2+. The basal, as well as the veratridine-stimulated, uptake of guanidinium was inhibited by the cholinergic antagonists (+)-tubocurarine (Ki = 50 to 500 nM) and atropine (Ki = 5 to 30 microM) and the adrenergic antagonists phentolamine (Ki = 5 microM) and propranolol (Ki = 60 microM). The specificity of the inhibitory effects of these agents is stressed by the ineffectiveness of various other neurotransmitter antagonists. However, the corresponding ionophore in neuroblastoma cells (clone N1E-115) seems to be regulated differently. While phentolamine and propranolol inhibit the veratridine-activated uptake as in the hybrid cells, (+)-tubocurarine and atropine exert only a slight effect.
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PMID:Blockade by neurotransmitter antagonists of veratridine-activated ion channels in neuronal cell lines. 613 Jan 27

There were 150 children with neuroblastoma and 183 children with Wilms' tumor who received radiation therapy, orthovoltage up to 1967, and cobalt therapy thereafter. In all except two cases, radiation therapy crossed the midline. Of all of the children treated, 13 required spinal fusion. There were six with Wilms' tumor; three had kyphosis; and three had scoliosis. Nine fusions were done with three pseudoarthroses, one broken rod, and two hook pullouts. There were seven with neuroblastoma, of whom five had kyphosis and two had scoliosis. Nineteen spinal fusions were done on these seven patients for neuroblastoma; two developed paraplegia; seven had pseudoarthroses; two had broken rods; and one had infection. Complications were attributed to laminectomies (five of seven) and high orthovoltage dosage (3680 rad), causing bone death and destroyed bone growth, with resultant infantile-size spines. The authors continue to follow up postradiation patients and observe rapid deterioration of kyphosis and scoliosis during the adolescent growth spurt. The authors now recommend early and extensive combined two-stage, long anterior and posterior fusions for kyphosis of 35 degrees and over, and a posterior fusion with Harrington rod instrumentation with extensive bone grafting is done for early (35 degrees) pure scoliosis. Postoperative immobilization is much longer than for regular spine fusions--at least one year.
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PMID:Results of spinal fusion for radiation scoliosis. 630 Oct 77

The metabolism of Ca2+ was studied in a neuronal model system, the clonal mouse neuroblastoma x rat glioma hybrid cell line 108CC5. 1. Homogenates of the hybrid cells exhibit a specific activity of Ca2+-ATPase considerably higher than that of homogenates of the parental cells. 2. Uptake and release of 45Ca2+ by the hybrid cells display two and three distinct phases, respectively, and indicate that 40--50% of the cell-associated Ca2+ is located at the cell surface. 3. The influx of 45Ca2+ is insignificantly affected by Mg2+ or Na+, slightly diminished by Ba2+ or Sr2+, strongly inhibited by La3+, Co2+ or prenylamine, and considerably enhanced by high (i.e., depolarizing) concentrations of K+. The efflux of 45Ca2+ is reduced by La3+. 4. The hybrid cells tend to maintain Ca2+ homeostasis with an overall cellular Ca2+ concentration of 0.5--0.7 mM. At 1.8 mM Ca2+ in the medium this implies the necessity of an extrusion pump in the plasma membrane. 5. A reduction in the hybrid cells of the level of ATP is paralleled by a decline in the content of Ca2+. This can only be explained by the existence of energy-dependent intracellular Ca2+ stores that effectively compete for Ca2+ with a Ca2+ pump located in the plasma membrane. The internal stores are not identical with the mitochondria because mitochondrial inhibitors hardly change Ca2+ metabolism. 6. Micromolar concentrations of the ionophore A23187 can switch off the internal Ca2+ stores without affecting considerably the influx of Ca2+ through the plasma membrane. 7. With switched-off Ca2+ stores it is possible to increase the cellular Ca2+ content distinctly and to bring it back again to the control values in an ATP-dependent manner, i.e. to demonstrate the action of a Ca2+-extrusion pump in the plasma membrane. 8. Under some conditions active extrusion of Ca2+ depends not only on ATP but also on the presence of extracellular Na+. 9. Similar results as with hybrid cells are also obtained with rat glioma cells. The methodology of combining energy deprivation with the application of the ionophore A23187 is possibly generally applicable to obtain insight into the Ca2+ metabolism of various cell types.
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PMID:Uptake and energy-dependent extrusion of calcium in neural cells in culture. 644 79

Kinetic analyses were made on intracellular Na+-dependent Ca2+ uptake by myocardial cells and neuroblastoma cells (N-18 strain) in culture. Cells loaded with various concentrations of Na+ could be prepared by incubating them in Ca2+-free medium containing various concentrations of Na+. Cells pre-loaded with various concentrations of Na+ were incubated in medium containing Ca2+ and 45Ca. The resulting 45Ca uptake by the two types of cell depended greatly on the initial intracellular concentrations of Na+. Lineweaver-Burk plots of the initial rate of Ca2+ uptake against the external concentration of Ca2+ fitted well to straight lines obtained by linear regression (r greater than 0.95). This result shows that Ca2+ uptake by the two types of cell was achieved by a carrier-mediated transport system. This Na+-dependent Ca2+ uptake was accompanied by Na+ release and the ratio of Na+ release to Ca2+ uptake was close to 3 : 1. A comparison of the kinetic data between myocardial cells and N-18 cells suggested that N-18 cells possess a carrier showing the same properties as that of myocardial cells, i.e.: (1) a similar dependency on the intracellular concentration of Na+; (2) the coincidence of the apparent Michaelis constants for Ca2+ (0.1 mM); (3) the similarities of the Ki values for Co2+, Sr2+ and Mg2+ (Co2+ less than Sr2+ less than Mg2+) and (4) a similar dependency on pH. However, the maximal initial rate, V, of N-18 cells was about 1/100 that of myocardial cells. The rate of Na+-dependent Ca2+ uptake by non-excitable cells was much lower than that by myocardial cells.
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PMID:Kinetic studies on sodium-dependent calcium uptake by myocardial cells and neuroblastoma cells in culture. 678 64

The effects of various Ca2+ channel agonists and antagonists on tumor cell growth were investigated using U-373 MG human astrocytoma and SK-N-MC human neuroblastoma cell lines. Classical Ca2+ channel antagonists, verapamil, nifedipine, and diltiazem, and inorganic Ca2+ channel antagonists, Ni2+ and Co2+, inhibited growth of these tumor cells in a dose-dependent manner. Except Ni2+, these Ca2+ channel antagonists did not induce a significant cytotoxicity, suggesting that the growth-inhibitory effects of these drugs may be the result of the influence on the proliferative signaling mechanisms of these tumor cells. In contrast, Bay K-8644, a Ca2+ channel agonist, neither enhanced the growth of tumor cells nor increased intracellular Ca2+ concentration, indicating that voltage-sensitive Ca2+ channels may not be involved in tumor cell proliferation. Moreover, growth-inhibitory concentrations of Ca2+ channel antagonists significantly blocked agonist (carbachol or serum)-induced intracellular Ca2+ mobilization, which was monitored using Fura-2 fluorescence technique. These results suggest that the inhibition of the growth of human brain tumor cells induced by Ca2+ channel antagonists may not be the result of interaction with Ca2+ channels, but may be the result of the interference with agonist-induced intracellular Ca2+ mobilization, which is an important proliferative signaling mechanism.
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PMID:Inhibition of cell growth and intracellular Ca2+ mobilization in human brain tumor cells by Ca2+ channel antagonists. 752 51

1. The ability of various divalent metal ions to substitute for Ca2+ in activating distinct types of Ca(2+)-dependent K+ [K+(Ca2+)] channels has been investigated in excised, inside-out membrane patches of human erthrocytes and of clonal N1E-115 mouse neuroblastoma cells using the patch clamp technique. The effects of the various metal ions have been compared and related to the effects of Ca2+. 2. At concentrations between 1 and 100 microM Pb2+, Cd2+ and Co2+ activate intermediate conductance K+(Ca2+) channels in erythrocytes and large conductance K+(Ca2+) channels in neuroblastoma cells. Pb2+ and Co2+, but not Cd2+, activate small conductance K+(Ca2+) channels in neuroblastoma cells. Mg2+ and Fe2+ do not activate any of the K+(Ca2+) channels. 3. Rank orders of the potencies for K+(Ca2+) activation are Pb2+, Cd2+ > Ca2+, Co2+ >> Mg2+, Fe2+ for the intermediate erythrocyte K+(Ca2+) channel, and Pb2+, Cd2+ > Ca2+ > Co2+ >> Mg2+, Fe2+ for the small, and Pb2+ > Ca2+ > Co2+ >> Cd2+, Mg2+, Fe2+ for the large K+(Ca2+) channel in neuroblastoma cells. 4. At high concentrations Pb2+, Cd2+, and Co2+ block K+(Ca2+) channels in erythrocytes by reducing the opening frequency of the channels and by reducing the single channel amplitude. The potency orders of the two blocking effects are Pb2+ > Cd2+, Co2+ >> Ca2+, and Cd2+ > Pb2+, Co2+ >> Ca2+, respectively, and are distinct from the potency orders for activation. 5. It is concluded that the different subtypes of K+(Ca2+) channels contain distinct regulatory sites involved in metal ion binding and channel opening. The K+(Ca2+) channel in erythrocytes appears to contain additional metal ion interaction sites involved in channel block.
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PMID:Differential effects of heavy metal ions on Ca(2+)-dependent K+ channels. 764 Dec 41


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