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Phosphorylation of voltage‐gated ion channels in rat olfactory receptor neurons
Author(s) -
Wetzel Christian H.,
Spehr Marc,
Hatt Hanns
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01722.x
Subject(s) - cyclic nucleotide gated ion channel , chemistry , olfactory receptor , ion channel , second messenger system , microbiology and biotechnology , protein kinase a , biophysics , biology , signal transduction , receptor , neuroscience , phosphorylation , cyclic nucleotide , biochemistry , nucleotide , gene
In olfactory receptor neurons (ORNs), ligand–odorant receptor interactions cause G protein‐mediated activation of adenylate cyclase and a subsequent increase in concentration of the intracellular messenger cAMP. Odorant‐evoked elevation in cAMP is thought to directly activate a cation‐selective cyclic nucleotide‐gated channel, which causes external Ca 2+ influx, leading to membrane depolarization and the generation of action potentials. Our data show that in freshly dissociated rat ORNs, odorant‐induced elevation in cAMP also activates cAMP‐dependent protein kinase (PKA), which is then able to phosphorylate various protein targets in the olfactory signal transduction pathway, specifically voltage‐gated sodium and calcium channels. The presence of PKI (PKA inhibitor peptide) blocked the modulatory action of cAMP on voltage‐gated ion channels. By modulating the input/output properties of the sensory neurons, this mechanism could take part in the complex adaptation process in odorant perception. In addition, we found modulation of voltage‐gated sodium and calcium channel currents by 5‐hydroxytryptamine and the dopamine D 1 receptor agonist SKF 38393. These findings suggest that in situ ORNs might also be a target for efferent modulation.