Abstract
Abstract— 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 [3H]quinuclidinyl benzilate ([3H]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 [3H]deoxy‐d‐glucose ([3H]DG) uptake and retention; (2) rate of cell division; (3) transport, measured by [3H]valine and [3H]uridine uptake; (4) RNA biosynthesis, measured by [3H]uridine incorporation; (5) protein biosynthesis, measured by [3H]valine and [35S]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 mm for 24 h) also caused a decrease in [3H]QNB binding levels, but chronic stimulation of α‐adrenergic, opiate, prostaglandin E1, and prostaglandin F2α 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.
Original language | English (US) |
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Pages (from-to) | 1099-1108 |
Number of pages | 10 |
Journal | Journal of Neurochemistry |
Volume | 37 |
Issue number | 5 |
DOIs | |
State | Published - Jan 1 1981 |
Keywords
- 2
- Cell culture
- d
- Deoxy
- glucose
- Neuron
- Phosphatidylinositol
- Synaptic plasticity
ASJC Scopus subject areas
- Biochemistry
- Medicine(all)
- Cellular and Molecular Neuroscience