NDLI: Muscarinic Inhibition of Hippocampal and Striatal Adenylyl Cyclase is Mainly Due to the M$

Content Provider	Springer Nature Link
Author	Sánchez, Gonzalo Colettis, Natalia Vázquez, Pablo Cerveñansky, Carlos Aguirre, Alejandra Quillfeldt, Jorge A. Jerusalinsky, Diana Kornisiuk, Edgar
Copyright Year	2009
Abstract	The five muscarinic acetylcholine receptors (M$_{1}$–M$_{5}$) are differentially expressed in the brain. M$_{2}$ and M$_{4}$ are coupled to inhibition of stimulated adenylyl cyclase, while M$_{1}$, M$_{3}$ and M$_{5}$ are mainly coupled to the phosphoinositide pathway. We studied the muscarinic receptor regulation of adenylyl cyclase activity in the rat hippocampus, compared to the striatum and amygdala. Basal and forskolin-stimulated adenylyl cyclase activity was higher in the striatum but the muscarinic inhibition was much lower. Highly selective muscarinic toxins MT1 and MT2—affinity order M$_{1}$ ≥ M$_{4}$ >> others—and MT3—highly selective M$_{4}$ antagonist—did not show significant effects on basal or forskolin-stimulated cyclic AMP production but, like scopolamine, counteracted oxotremorine inhibition. Since MTs have negligible affinity for M$_{2}$, M$_{4}$ would be the main subtype responsible for muscarinic inhibition of forskolin-stimulated enzyme. Dopamine stimulated a small fraction of the enzyme (3.1% in striatum, 1.3% in the hippocampus). Since MT3 fully blocked muscarinic inhibition of dopamine-stimulated enzyme, M$_{4}$ receptor would be responsible for this regulation.
Starting Page	1363
Ending Page	1371
Page Count	9
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	34
Issue Number	8
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2009-02-04
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Muscarinic acetylcholine receptor Adenylyl cyclase Muscarinic toxins Hippocampus Striatum Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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