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neuroblastoma/scopolamine
Veza se sprema u međuspremnik
Page 1 od 52 rezultati
Non-muscarinic effects of scopolamine on N1E-115 neuroblastoma cells.
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Membrane effects of scopolamine on N1E-115 neuroblastoma cells were studied using intracellular recording techniques. Scopolamine in concentrations of 50 nM-1 microM induced a depolarization together with a decreased cell input resistance. This response had a reversal potential at +10 to +20 mV in a
Neuroprotection of SAK3 on scopolamine-induced cholinergic dysfunction in human neuroblastoma SH-SY5Y cells.
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Alzheimer's disease (AD) is the most common type of senile dementia. A number of factors have been proposed regarding pathology of AD, such as presence of β-amyloid, and cholinergic and oxidative stress. SAK3 (ethyl
Neuroprotection of N-benzylcinnamide on scopolamine-induced cholinergic dysfunction in human SH-SY5Y neuroblastoma cells.
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Alzheimer's disease, a progressive neurodegenerative disease, affects learning and memory resulting from cholinergic dysfunction. Scopolamine has been employed to induce Alzheimer's disease-like pathology in vivo and in vitro through alteration of cholinergic system. N-benzylcinnamide (PT-3),
Melandrii Herba Extract Attenuates H₂O₂-Induced Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells and Scopolamine-Induced Memory Impairment in Mice.
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Oxidative stress plays a significant role in the etiology of a variety of neurodegenerative diseases. In this study, we found that Melandrii Herba extract (ME) attenuated oxidative-induced damage in cells. Mechanistically, ME exhibited protection from H₂O₂-induced neurotoxicity via caspase-3
DADS Analogues Ameliorated the Cognitive Impairments of Alzheimer-Like Rat Model Induced by Scopolamine.
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The development of agents that affect two or more relevant targets has drawn considerable attention in treatment of AD. Diallyl disulfide (DADS), an active principle of garlic, has been reported to prevent APP processing by amyloidogenic pathway. Recently, we have reported a new series of DADS
Essential fatty acid deficiency in cultured SK-N-SH human neuroblastoma cells.
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SK-N-SH neuroblastoma cells grown under standard culture conditions contain significant amounts of Mead acid (20:3 omega 9) in phospholipids, indicating essential fatty acid (EFA) deficiency. The amount of esterified 20:3 omega 9 was augmented by growth in a chemically defined EFA-free medium,
The effect of sodium channel activators on muscarinic receptors of neuroblastoma cells.
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Incubation of neuroblastoma NIE 115 cells with veratrine leads to an apparent reduction in the number of muscarinic acetylcholine receptors assayed by [3H]scopolamine methyl chloride binding. No true down-regulation of the receptors occurs but a component of veratrine with muscarinic receptor
Recognition of muscarinic cholinergic receptors in human SK-N-SH neuroblastoma cells by quaternary and tertiary ligands is dependent upon temperature, cell integrity, and the presence of agonists.
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The recognition of muscarinic cholinergic receptors (mAChRs) in human SK-N-SH neuroblastoma cells by hydrophilic (quaternary) and lipophilic (tertiary) ligands has been examined. When quiescent cells were incubated at 37 degrees, the same maximum number of mAChRs was revealed by antagonists that
Differential sensitivity of phosphoinositide and cyclic GMP responses to short-term regulation by a muscarinic agonist in mouse neuroblastoma cells. Correlation with down-regulation of cell surface receptors.
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Short-term agonist-induced loss of cell surface muscarinic receptors and desensitization of receptor-mediated cyclic GMP (cGMP) formation and phosphoinositide hydrolysis were examined in mouse neuroblastoma cells (clone N1E-115) in suspension. This treatment resulted in a time-dependent reduction of
SK & F 96365 inhibits carbachol-induced phosphoinositide turnover in human neuroblastoma SH-SY5Y and rat cerebellar granule cells.
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SK & F 96365, a receptor-mediated Ca2+ entry inhibitor, has been reported to inhibit Ca2+ responses to various agonists without affecting internal Ca2+ release and phosphoinositide turnover. Since muscarinic acetylcholine receptor-mediated phosphoinositide turnover shows a marked dependence on
Neuroprotective effect of arctigenin via upregulation of P-CREB in mouse primary neurons and human SH-SY5Y neuroblastoma cells.
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Arctigenin (Arc) has been shown to act on scopolamine-induced memory deficit mice and to provide a neuroprotective effect on cultured cortical neurons from glutamate-induced neurodegeneration through mechanisms not completely defined. Here, we investigated the neuroprotective effect of Arc on
Intracellular distribution of functional M(1) -muscarinic acetylcholine receptors in N1E-115 neuroblastoma cells.
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Signaling by muscarinic agonists is thought to result from the activation of cell surface acetylcholine receptors (mAChRs) that transmit extracellular signals to intracellular systems. In N1E-115 neuroblastoma cells, we detected both plasma membrane and intracellular M(1) -mAChRs using both
Reduction of muscarinic receptor density and of guanine nucleotide-stimulated phosphoinositide hydrolysis in human SH-SY5Y neuroblastoma cells following long-term treatment with 12-O-tetradecanoylphorbol 13-acetate or mezerein.
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The actions of tumor promoters on the coupling of muscarinic receptors to the hydrolysis of inositol lipids and the generation of Ca2+ signals were examined in the human neuroblastoma SH-SY5Y cell line. Pretreatment of SH-SY5Y cells with 50 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) for 5 days
Muscarinic acetylcholine receptors in neuroblastoma cells: lack of effect of Veratrum alkaloids on receptor number.
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The effect of compounds that activate sodium channels on the number of muscarinic acetylcholine receptors in neuroblastoma NIE 115 cells has been investigated. The cells were used in electrically unexcitable ("control" cells) and excitable ("differentiated" cells) states. Although receptor assays
Mixed competitive and allosteric antagonism by gallamine of muscarinic receptor-mediated second messenger responses in N1E-115 neuroblastoma cells.
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The antagonistic effects of gallamine on muscarinic receptor-linked responses were investigated in N1E-115 neuroblastoma cells. M1 muscarinic receptor-mediated phosphoinositide hydrolysis induced by carbamylcholine was antagonized by gallamine, with a Ki value of 33 microM. By comparison, gallamine
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