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Science 5 February 1993:
Vol. 259. no. 5096, pp. 825 - 829
DOI: 10.1126/science.8381559
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Articles

Science, Vol 259, Issue 5096, 825-829
Copyright © 1993 by American Association for the Advancement of Science

articles

Beta-adrenergic receptor kinase-2 and beta-arrestin-2 as mediators of odorant-induced desensitization

TM Dawson, JL Arriza, DE Jaworsky, FF Borisy, H Attramadal, RJ Lefkowitz, and GV Ronnett

Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD 21205.

beta-Adrenergic receptor kinase (beta ARK) and beta-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms beta ARK-2 and beta-arrestin-2 are highly enriched in and localized to the dendritic knobs and cilia of the olfactory receptor neurons where the initial events of olfactory signal transduction occur. Odorants induce a rapid and transient elevation of adenosine 3',5'-monophosphate (cAMP), which activates a nonspecific cation channel and produces membrane depolarization. Preincubation of rat olfactory cilia with antibodies raised against beta ARK-2 and beta-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that beta ARK-2 and beta-arrestin-2 mediate agonist-dependent desensitization in olfaction.


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