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)

The regulation of glycogen metabolism in C-6 astrocytoma and C-1300 neuroblastoma cells in culture has been investigated. Two modes of control of glycogen metabolism appear to be operative. The regulation of intracellular glycogen concentrations and the predominant forms of glycogen phosphorylase and glycogen synthase vary with (a) the available energy supply, and (b) altered intracellular concentration of cyclic adenosine 3':5'-monophosphate (cyclic AMP). Both cell lines respond to glucose in the medium; when glucose levels are high, glycogen is synthesized, glycogen phosphorylase a decreases, and glycogen synthase a increases. When glucose in the medium decreases to a critical level, the phosphorylase a increases and glycogen concentrations in the cells decrease in aprallel with the medium glucose. The critical glucose concentration is 2.5 mM for the astrocytoma cells and 4 mM for the neuroblastoma cells. Insulin promotes the conversion of phosphorylase to the b form and synthase to the a form in both cell lines. All of these changes occur without alteration in the intracellular cyclic AMP concentrations. When cyclic AMP concentrations are increased in either cell line, phosphorylase a is increased, synthase a is decreased, and glycogen concentrations decrease. Isobutyl methylxanthine is effective in promoting glycogenolysis in both cell lines. Norepinephrine is effective with the astrocytoma cells, and prostaglandin E1 is effective with the neuroblastoma cells.
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PMID:Regulation of glycogen metabolism in astrocytoma and neuroblastoma cells in culture. 17 53

Addition of 1 micronM 1-norepinephrine to cultures of C6TK- rat glioma cells caused a 2-fold increase in specific activity of the glial-specific enzyme 2':3'-cyclic nucleotide 3'-phosphohydrolase (nucleoside-2':3'-cyclic-phosphate 3'-nucleotidohydrolase, EC 3.1.4.16). Specific activity could also be stimulated by analogues of 3':5'-cyclic AMP, and the effect of norepinephrine could be blocked by beta-adrenergic receptor antagonists but not by alpha-adrenergic antagonists. Norepinephrine or cyclic AMP analogues also increased the specific activity of this enzyme in other clones of glioma and Schwannoma cells and in glioma X neuroblastoma cell hybrids. These results show that the stimulatory effect of norepinephrine on cyclic AMP concentrations in glioma cells leads ultimately to a stimulation of glial-specific cell funtion.
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PMID:Norepinephrine induces glial-specific enzyme activity in cultured plasma glioma cells. 20 Sep 19

The effect of polyamines on the cellular concentrations of cyclic AMP was studied. It was shown that 1 microM-spermine caused a decrease in cyclic AMP in chick-embryo heart cells, chick-embryo fibroblasts, neuroblastoma, glioma and neuroblastoma-glioma hybrid cells, grown in culture. A similar decrease was observed when polyamines were added to cells in the presence of a phosphodiesterase inhibitor or after stimulating the cells with various hormones. Noradrenaline was used in cultures of heart cells, prostaglandin E1 and adenosine for neuroblastoma and neuroblastoma-glioma hybrids, whereas isoproterenol was used for the stimulation of glioma cells. Polyamines at higher concentrations were either without effect or caused a slight increase in cyclic AMP. Spermidine (10 microM) also caused a decrease in cellular cyclic AMP, as did 0.1 microM-putrescine. It is suggested that the effect of polyamines on cellular cyclic AMP may be explained by the effect of these polycations on the activity of cellular phosphodiesterase.
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PMID:Polyamines and cellular adenosine 3' :5'-cyclic monophosphate. 22 23

High-threshold (HVA) Ca2+ channels of human neuroblastoma IMR32 cells were effectively inhibited by noradrenaline. At potentials between -20 mV and +10 mV, micromolar concentrations of noradrenaline induced a 50%-70% depression of HVA Ba2+ currents and a prolongation of their activation kinetics. Both effects were relieved at more positive voltages or by applying strong conditioning pre-pulses (facilitation). Facilitation restored the rapid activation of HVA channels and recruited about 80% of the noradrenaline-inhibited channels at rest. Re-inhibition of Ca2+ channels after facilitation was slow (tau r 36-45 ms) and voltage-independent between -30 mV and -90 mV. The inhibitory action of noradrenaline was dose-dependent (IC50 = 84 nM), mediated by alpha 2-adrenergic receptors and selective for omega-conotoxin-sensitive Ca2+ channels, which represent the majority of HVA channels expressed by IMR32 cells. The action of noradrenaline was mimicked by intracellular applications of GTP[gamma S] and prevented by GDP[beta S] or by pre-incubation with pertussis toxin. The time course of noradrenaline inhibition measured during fast application (onset) and wash-out (offset) of the drug were independent of saturating agonist concentrations (10-50 microM) and developed with mean time constants of 0.56 s (tau on) and 3.6 s (tau off) respectively. The data could be simulated by a kinetic model in which a G protein is assumed to modify directly the voltage-dependent gating of Ca2+ channels. Noradrenaline-modified channels are mostly inhibited at rest and can be recruited in a steep voltage-dependent manner with increasing voltages.
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PMID:Voltage-dependent noradrenergic modulation of omega-conotoxin-sensitive Ca2+ channels in human neuroblastoma IMR32 cells. 133 78

The clonal human neuroblastoma cell line SK-N-SH-SY5Y was previously shown to express mu-opioid and alpha 2-adrenoceptors which are both negatively coupled to adenylyl cyclase. Because of the potential use of alpha 2-agonists in the treatment of narcotic dependence, we tested the interactions among he alpha 2-agonists, clonidine and norepinephrine, and morphine on AC in SH-SY5Y cells. Pretreatment with retinoic acid resulting in partial neuronal differentiation greatly enhanced the cells' sensitivity towards adenylyl cyclase stimulation by prostaglandin E1, and its inhibition by morphine and alpha 2-agonists. Norepinephrine (EC50 = 69 nM) maximally inhibited prostaglandin E1-stimulated cAMP accumulation (by approximately 83%), and the alpha 2-agonist yohimbine reversed these effects. Clonidine (EC50 = 32 nM) was a partial agonist, with 50 to 60% maximal inhibition. The combined effects of morphine (maximum approximately 70% inhibition) and norepinephrine exceeded the effect of either agent alone, yielding more than 90% inhibition of prostaglandin E1-stimulated cAMP accumulation. As previously reported for morphine, only a partial tolerance was observed for adenylyl cyclase inhibition by norepinephrine. Further, no cross-tolerance was observed between clonidine and morphine. The combined results indicate that mu-opioid receptors and an alpha 2-adrenoceptor subtype are colocalized on the same cells in SH-SY5Y culture, which hence serves as a model to study opioid-alpha 2-adrenergic interactions.
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PMID:Interaction among mu-opioid receptors and alpha 2-adrenoceptors on SH-SY5Y human neuroblastoma cells. 135 61

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 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

1. The effect of Lambert-Eaton myasthenic syndrome (LEMS) immunoglobulin G (IgG) on Ca2+ channels in undifferentiated mouse neuroblastoma x rat glioma hybrid cells (NG 108 15) was studied using the whole-cell patch clamp technique. 2. Sustained inward Ca2+ channel currents were evoked by depolarizing pulses from holding potentials of -80 and -40 mV, and were blocked by 5 microM-nitrendipine (L-type currents). Transient inward Ca2+ channel currents were activated from a holding potential of -80 mV by small depolarizing steps (T-type currents). Noradrenaline (10 microM) was without effect on transient currents. 3. LEMS IgG selectively reduced sustained (L-type) Ca2+ channel current amplitudes evoked from either holding potential used. In the presence of nitrendipine (5 microM), there was no significant effect of LEMS IgG on the remaining transient (T-type) Ca2+ channel current amplitudes. 4. Studies of the potential for maximal inward current indicated that voltage sensitivities of both L- and T-type Ca2+ channel current amplitudes were unaffected by LEMS IgG, whether recorded in the presence or absence of nitrendipine. LEMS IgG had no significant effect on the time-to-peak or decay of Ca2+ channel currents. 5. It is concluded that LEMS IgG acts selectively to cause functional loss of L-type, but not T-type, Ca2+ channels in NG 108 15 cells. Any effect of LEMS IgG on N-type channels (not present in these undifferentiated cells) was not studied here. LEMS IgG also acts at motor nerve terminal Ca2+ channels leading to muscle weakness. Thus antigenic similarities must exist between L-type channels in NG 108 15 cells and Ca2+ channels at motor nerve terminals.
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PMID:Selective action of myasthenic syndrome antibodies on calcium channels in a rodent neuroblastoma x glioma cell line. 216 58

The regulation of cytoplasmic pH (pHi) was examined in neuroblastoma X glioma hybrid cell-line cells (NG108-15 cells) using 2,7-biscarboxyethyl-5(6)-carboxyfluorescein. The pHi of NG108-15 cells suspended in nominally HCO-3-free, Na+-containing buffer could be reduced by the external application of acetate. The recovery of pHi to its resting value was blocked by the removal of extracellular Na+, by the addition of extra-cellular H+, and by the addition of analogs of amiloride selective for inhibition of Na+/H+ exchange. The rate of recovery of pHi from acid load exhibited an ionic selectivity of Na+ greater than Li+ much greater than K+, and no recovery was observed in N-methyl-D-glucamine+. Tetrodotoxin and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid had no effect on early pHi recovery. These data suggest that Na+/H+ exchange accounts primarily for the recovery of pHi in NG108-15 cells under our experimental conditions. Na+/H+ exchange in NG108-15 cells was accelerated by alpha 2-adrenergic receptors. Thus, (-)epinephrine, but not (+)epinephrine, elicited an intracellular alkalinization which was blocked by the alpha 2-adrenergic receptor selective antagonist yohimbine but not by the alpha 1-adrenergic receptor antagonist, prazosin, nor the beta-adrenergic antagonist, propranolol. Norepinephrine, clonidine, and the clonidine analog, UK-14304, also caused alkalinization of NG108-15 cells, whereas isoproterenol, a beta-adrenergic receptor agonist, and phenylephrine, a selective alpha 1-adrenergic receptor agonist, did not. Manipulations that blocked Na+/H+ exchange blocked the ability of alpha 2-adrenergic agonists to alkalinize the interior of NG108-15 cells without blocking the ability of these agonists to attenuate cAMP accumulation. These findings provide the first direct evidence of modulation of Na+/H+ exchange activity by a receptor linked to inhibition of adenylate cyclase and offer a possible mechanism whereby alpha 2-adrenergic receptors might influence cellular activity apart from changes in cyclic nucleotide metabolism.
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PMID:Alpha 2-adrenergic receptors accelerate Na+/H+ exchange in neuroblastoma X glioma cells. 288 87

The clinical manifestations of 253 neuroblastoma cases in childhood, treated in Denmark from 1943 to 1980, were reviewed. Most striking was the vagueness of symptoms in the majority of patients, only a few of whom exhibited the symptoms strongly suggestive of a neuroblastoma (i.e. the Horner syndrome, the watery diarrhoea syndrome, the dancing eye syndrome). The vagueness of the symptoms might have led to fatal procrastination of the diagnosis. The diagnostic delay has, however, no independent prognostic significance for survival in our patients (p = 0.09). The maximal tumour spread was recorded for all 253 patients, and the distribution of metastases was in accordance with the "soil-seed" hypothesis. The tumour spreads with equal frequency by local growth, by lymphatic vessels to distant lymph nodes, and by blood to bone. Only in widely disseminated tumours are metastases to the lungs, the meninges, the brain, and the reproductive organs seen to occur. Eighty-five percent of the patients, for whom data were available, excreted VMA above the normal value for their age, and 43% excreted Norepinephrine + Epinephrine (N + E) above normal levels. The excretion of both VMA and N + E was significantly correlated to stage, and thus to prognosis. Neither the level of VMA excretion nor the level of N + E had any bearing on the survival when age and stage were adjusted for. Serial VMA and N + E determinations show that patients with normal values for these parameters had significantly better prognosis than patients with elevated values during the first, second, third and fourth trimesters after the initiation of treatment. Increasing values in the individual patient were associated with a poor prognosis. We found no correlation between the initial leucocyte count and survival when age and stage were adjusted for.
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PMID:Signs, symptoms, metastatic spread and metabolic behavior of neuroblastomas treated in Denmark during the period 1943-1980. 363 7


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