M(2)/M(4)-muscarinic receptors mediate automodulation of acetylcholine outflow from mouse cortex

Acetylcholine outflow can be modulated through inhibitory presynaptic muscarinic autoreceptors. This study was to identify which subtype is involved in mouse cortex. Five muscarinic antagonists and their ability to elevate stimulation-induced (S-I) acetylcholine outflow were tested in the presence o...

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Bibliographic Details
Published in:Neuroscience letters 2000-06, Vol.287 (2), p.129-132
Main Authors: Iannazzo, L, Majewski, H
Format: Article
Language:English
Subjects:
Acetylcholine - metabolism
Alkaloids - metabolism
Alkaloids - pharmacology
Animals
Atropine - metabolism
Atropine - pharmacology
Autoreceptors - metabolism
Binding, Competitive - physiology
Cerebral Cortex - metabolism
Furans
Male
Mice
Muscarinic Antagonists - metabolism
Muscarinic Antagonists - pharmacology
Naphthalenes
Neostigmine - metabolism
Neostigmine - pharmacology
Parasympatholytics - metabolism
Parasympatholytics - pharmacology
Parasympathomimetics - metabolism
Parasympathomimetics - pharmacology
Piperidines - metabolism
Piperidines - pharmacology
Pirenzepine - analogs & derivatives
Pirenzepine - metabolism
Pirenzepine - pharmacology
Receptor, Muscarinic M2
Receptor, Muscarinic M4
Receptors, Muscarinic - metabolism
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Summary:Acetylcholine outflow can be modulated through inhibitory presynaptic muscarinic autoreceptors. This study was to identify which subtype is involved in mouse cortex. Five muscarinic antagonists and their ability to elevate stimulation-induced (S-I) acetylcholine outflow were tested in the presence of neostigmine, which decreased S-I outflow. The potency of each antagonist was determined, expressed as a ratio of the potency of each other antagonist and compared with the potency ratios of the antagonists for each of the defined muscarinic receptors (M(1)-M(4)), as recorded in the literature. Linear regression analysis revealed that the data fitted the M(2) (r(2)>0.97) and M(4) (r(2)>0.85) subtypes best, with no correlation for the M(1) and M(3) subtypes.
ISSN:0304-3940