Targeted gene deletion of the 5-HT3A receptor subunit produces an anxiolytic phenotype in mice.

Kelley, Stephen P. and Bratt, Alison M. and Hodge, Clyde W. (2003) Targeted gene deletion of the 5-HT3A receptor subunit produces an anxiolytic phenotype in mice. European Journal of Pharmacology, 461 (1). pp. 19-25. ISSN 0014-2999. (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided)

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Anxiety disorders are the most common psychiatric disorders. Typical medications used to treat patients are benzodiazepines or antidepressants that target serotonin (5-HT) activity. The ionotropic 5-HT3 receptor has emerged as a potential therapeutic target because selective antagonist compounds reduce anxiety in rodents, primates, and humans. 5-HT binds to the extracellular N-terminus of the 5-HT3A receptor subunit, but receptor activation is also enhanced by distinct allosteric sites. It is not known if specific molecular subunits of the 5-HT3 receptor modulate anxiety. To address this issue, we characterized anxiety-like behavior of mice with a targeted deletion of the 5-HT3A receptor subunit gene in the light/dark box, elevated plus maze, and novelty interaction animal models of anxiety. 5-HT3A null mice exhibited an anxiolytic behavioral phenotype that was highly correlated across behavioral measures. This evidence indicates that the 5-HT3A molecular subunit influences anxiety-like behavior. Pharmacotherapy that targets specifically the 5-HT3A receptor subunit may provide a novel treatment for anxiety disorders.

Item Type: Article
Uncontrolled keywords: 5-HT, (5-hydroxytryptamine; serotonin); 5-HT3A receptor; Anxiety; Animal model; (Mouse)
Subjects: Q Science > QP Physiology (Living systems)
R Medicine > RM Therapeutics. Pharmacology
Divisions: Faculties > Science Technology and Medical Studies > Medway School of Pharmacy
Depositing User: Stephen Kelley
Date Deposited: 29 Jun 2011 17:07
Last Modified: 23 Apr 2014 14:17
Resource URI: (The current URI for this page, for reference purposes)
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