Nicotinic Agonists Regulate တBungarotoxin Binding Sites Of Te671 Human Medulloblastoma Cells

Department

neurobiology

Document Type

Article

Abstract

Abstract: The TE671 human medulloblastoma cell line expresses a variety of characteristics of human neurons. Among these characteristics is the expression of membrane‐bound high‐affinity binding sites for α‐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 d‐tubocurarine, induced up to a fivefold increase in the density of radiolabeled toxin binding sites in crude membrane fractions. This effect was blocked by co‐incubation with the nicotinic antagonists d‐tubocurarine and decamethonium, but not by mecamylamine or by muscarinic antagonists. Following a 10–13 h lag phase upon removal of agonist, recovery of the up‐regulated sites to control values occurred within an additional 10–20 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 nicotine‐induced up‐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, nicotine‐induced receptor blockade does not appear to be involved. Copyright © 1988, Wiley Blackwell. All rights reserved

Publication Date

1-1-1988

Publication Title

Journal of Neurochemistry

ISSN

00223042

Volume

50

Issue

4

First Page

1272

Last Page

1278

Digital Object Identifier (DOI)

10.1111/j.1471-4159.1988.tb10604.x

This document is currently not available here.

Share

COinS