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Originally published In Press as doi:10.1074/jbc.M106744200 on December 20, 2001

J. Biol. Chem., Vol. 277, Issue 13, 10869-10875, March 29, 2002
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Nicotine Preconditioning Antagonizes Activity-dependent Caspase Proteolysis of a Glutamate Receptor*

Erin L. Meyer, Lorise C. Gahring, and Scott W. RogersDagger

From the Salt Lake City Veterans Affairs-Geriatrics Research, Education, and Clinical Center and the University of Utah School of Medicine, Salt Lake City, Utah 84132

Neuronal excitation is required for normal brain function including processes of learning and memory, yet if this process becomes dysregulated there is reduced neurotransmission and possibly death through excitotoxicity. Nicotine, through interaction with neuronal nicotinic acetylcholine receptors, possesses the ability to modulate neurotransmitter systems through numerous mechanisms that define this critical balance. We examined the modulatory role of nicotine in primary mixed cortical neuronal-glial cultures on activity-dependent caspase cleavage of a glutamate receptor, GluR1. We find that GluR1, but not GluR2 or GluR3, is a substrate for agonist (alpha -amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid)-initiated rapid proteolytic cleavage at aspartic acid 865 through the activation of caspase 8-like activity that is independent of membrane fusion and is not coincident with apoptosis. Dose-dependent nicotine preconditioning for 24 h antagonizes agonist-initiated caspase cleavage of GluR1 through a mechanism that is coincident with desensitization of both nAChRalpha 4beta 2 and nAChRalpha 7 receptors and the delayed activation of a caspase 8-like activity. The modulation of GluR1 agonist-initiated caspase-mediated cleavage by nicotine preconditioning offers a novel insight into how this agent can impart its numerous effects on the nervous system.

* This work was supported by National Institutes of Health Grant NIH-NS35181 and the Val A. Browning Foundation.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.

Dagger To whom correspondence should be addressed: University of Utah School of Medicine, Dept. of Neurobiology and Anatomy, 50 North Medical Dr., Salt Lake City, UT 84132. Tel.: 801-585-6339; Fax: 801-585-3884; E-mail: Scott.Rogers@HSC.UTAH.EDU.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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