β-Adrenergic receptor kinase (βARK) and β-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms βARK-2 and β-ar-restin-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 βARK-2 and β-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that βARK-2 and β-arrestin-2 mediate agonist-dependent desensitization in olfaction.
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