Premium
Muscarinic Acetylcholine Receptors in Neuroblastoma Cells: Lack of Effect of Veratrum Alkaloids on Receptor Number
Author(s) -
Milligan Graeme,
Strange Philip G.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb06675.x
Subject(s) - veratridine , muscarinic acetylcholine receptor , chemistry , muscarinic acetylcholine receptor m3 , muscarinic acetylcholine receptor m1 , receptor , muscarinic acetylcholine receptor m2 , muscarinic acetylcholine receptor m5 , acetylcholine , endocrinology , tetrodotoxin , acetylcholine receptor , muscarinic acetylcholine receptor m4 , pharmacology , medicine , sodium channel , biology , sodium , biochemistry , organic chemistry
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 using a single concentration of the radioligand [ 3 H]scopolamine methyl chloride indicated a loss of receptors after a 6‐h incubation of cells with veratrine, no true loss of receptors was seen with any of the compounds tested (veratridine, veratrine, aconitine) when full saturation analyses were performed in either control or differentiated cells. The apparent receptor loss seen with veratrine was due to a muscarinic receptor‐active component of veratrine (not veratridine) occluded by the cells and released into the binding assays ùpon cell breakage. Veratridine and aconitine have a very low affinity for muscarinic acetylcholine receptors, and the binding of carbamoylcholine to the receptors is unaffected by tetrodotoxin, so that there is no evidence in this system for interaction between muscarinic receptors and sodium channels.