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Specificity of Muscarinic Acetylcholine Receptor Regulation by Receptor Activity
Author(s) -
Siman Robert G.,
Klein William L.
Publication year - 1981
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.1471-4159.1981.tb04659.x
Subject(s) - muscarinic acetylcholine receptor , endocrinology , muscarinic acetylcholine receptor m3 , medicine , muscarinic acetylcholine receptor m1 , muscarinic acetylcholine receptor m5 , carbachol , receptor , stimulation , chemistry , acetylcholine , biology , biochemistry
— Regulation of muscarinic acetylcholine receptor concentration by receptor activity in neuron‐like NG108‐15 hybrid cells is a highly specific process. Receptor levels, monitored by binding of [ 3 H]quinuclidinyl benzilate ([ 3 H]QNB), decreased 50‐75% following 24‐h incubation of cells with muscarinic agonists, but none of the following cellular processes was altered by this chronic receptor stimulation: (1) glycolytic energy metabolism, measured by [ 3 H]deoxy‐ d ‐glucose ([ 3 H]DG) uptake and retention; (2) rate of cell division; (3) transport, measured by [ 3 H]valine and [ 3 H]uridine uptake; (4) RNA biosynthesis, measured by [ 3 H]uridine incorporation; (5) protein biosynthesis, measured by [ 3 H]valine and [ 35 S]methionine incorporation into total protein and into protein fractions obtained by polyacrylamide gel electrophoresis. In contrast, chronic stimulation did cause a threefold decrease in the capacity of carbachol to stimulate phosphatidylinositol (PI) turnover, a receptor‐mediated response. In addition to cholinomimetics, the neuroeffector adenosine (1 m m for 24 h) also caused a decrease in [ 3 H]QNB binding levels, but chronic stimulation of α ‐adrenergic, opiate, prostaglandin E 1 , and prostaglandin F 2α receptors found on NG108‐15 cells caused no changes. The data indicate that loss of muscarinic receptors caused by receptor stimulation is not a consequence of fundamental changes evoked in overall cellular physiology but reflects a specific regulation of cholinoceptive cell responsiveness.