Nicotinic Agonists Regulate Î±Â€Bungarotoxin Binding Sites Of Te671 Human Medulloblastoma Cells
Abstract: The TE671 human medulloblastoma cell line expresses a variety of characteristics of human neurons. Among these characteristics is the expression of membraneâ€bound highâ€affinity binding sites for Î±â€bungarotoxin, which is a potent antagonist of functional nicotinic acetylcholine receptors on these cells. These toxin binding sites represent a class of nicotinic receptor isotypes present in mammalian brain. Treatment of TE671 cells during proliferative growth phase with nicotine or carbamylcholine, but not with muscarine or dâ€tubocurarine, induced up to a fivefold increase in the density of radiolabeled toxin binding sites in crude membrane fractions. This effect was blocked by coâ€incubation with the nicotinic antagonists dâ€tubocurarine and decamethonium, but not by mecamylamine or by muscarinic antagonists. Following a 10â€“13 h lag phase upon removal of agonist, recovery of the upâ€regulated sites to control values occurred within an additional 10â€“20 h. These studies indicate that the expression of functional nicotinic acetylcholine receptors on TE671 cells is subject to regulation by nicotinic agonists. Studies of the murine CNS have consistently indicated nicotineâ€induced upâ€regulation of nicotinic acetylcholine receptors, thereby supporting the identification of the toxin binding site on these cells as the functional nicotinic receptor. Although a mechanism for this effect is not apparent, nicotineâ€induced receptor blockade does not appear to be involved. Copyright Â© 1988, Wiley Blackwell. All rights reserved
Journal of Neurochemistry
Digital Object Identifier (DOI)
Siegel, Hal N. and Lukas, Ronald J., "Nicotinic Agonists Regulate Î±Â€Bungarotoxin Binding Sites Of Te671 Human Medulloblastoma Cells" (1988). Translational Neuroscience. 259.