Premium
Genotypic m3‐Muscarinic Receptors Preferentially Inhibit M‐currents in DNA‐transfected NG108‐15 Neuroblastoma × Glioma Hybrid Cells
Author(s) -
Robbins J.,
Caulfield M. P.,
Higashida H.,
Brown D. A.
Publication year - 1991
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1991.tb01678.x
Subject(s) - muscarinic acetylcholine receptor , transfection , muscarine , acetylcholine , microbiology and biotechnology , muscarinic acetylcholine receptor m1 , neuroblastoma , receptor , muscarinic acetylcholine receptor m2 , chemistry , carbachol , pirenzepine , biology , cell culture , endocrinology , biochemistry , genetics
The ability of different genotypic muscarinic acetylcholine receptors (mAChR) to inhibit the neural K + ‐current, I M , was assessed in clones of NG108‐15 mouse neuroblastoma × rat glioma cells transfected with DNA for the genomic mAChRs ml –4 using tight‐seal, whole‐cell patch clamp recording. No significant inhibition of I M was seen in native (non‐transfected) cells, or in m2 or m4 DNA‐transfected cells at concentrations of acetylcholine up to 1 mM or muscarine up to 100 μM. Both acetylcholine and muscarine produced complete inhibition of I M in m3 DNA‐transfected cells, but only partial (50–60%) inhibition in m1 DNA‐transfected cells at maximally effective concentrations. This difference could not be explained by differences in mAChR number, as measured by radioligand binding and was not eliminated by adding GTP to the pipette. It is concluded that genotypic m3 receptors couple most effectively to I M and that this may explain previously reported instances of pirenzepine‐resistant I M ‐inhibition.