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J. Biol. Chem., Vol. 276, Issue 19, 15850-15853, May 11, 2001
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From the Department of Pharmacology, University of Washington
School of Medicine, Seattle, Washington 98195-7750
Muscarinic acetylcholine receptors (mAChR) in the
central nervous system are involved in learning and memory, epileptic
seizures, and processing the amyloid precursor protein. The
M1 receptor is the predominant mAChR subtype in the
cortex and hippocampus. Although the five mAChR fall into two broad
functional groups, all five subtypes, when expressed in recombinant
systems, can activate the mitogen-activated protein kinase (MAPK)
pathway. The MAPK pathway has been implicated in learning and memory,
amyloid protein processing, and neuronal plasticity. We used
M1 knock-out mice to determine the role of this receptor
subtype in signal transduction in the mouse forebrain. In primary
cortical cultures from mice lacking the M1 mAChR,
agonist-stimulated phosphoinositide hydrolysis was reduced by more than
60% compared with cultures from wild type mice. Although muscarinic
agonists induced robust activation of MAPK in cortical cultures from
wild type mice, mAChR-mediated activation of MAPK was virtually absent
in cultures from M1-deficient mice. These results indicate
that the M1 mAChR is the major subtype that mediates
activation of phospholipase C and MAPK in mouse forebrain.
The M1 Receptor Is Required for Muscarinic Activation
of Mitogen-activated Protein (MAP) Kinase in Murine Cerebral
Cortical Neurons*
*
This work was supported by National Institutes of Health
Grant NS26920.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Pharmacology,
P. O. Box 357750, Univ. of Washington School of Medicine, Seattle, WA 98195-7750. Tel.: 206-543-9457; Fax: 206-616-4230; E-mail: nathanso@u.washington.edu.
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