Abstract
A biochemical model is developed for the receptor, G-protein and effector (RGE) steps of olfactory signal transduction in the cilia of the vertebrate olfactory receptor neurons (ORNs). It describes the steps from odorant binding to activation of the effector enzyme, which catalyzes the conversion of ATP to cAMP. In the cilia of the olfactory receptor neurons (ORNs), cAMP regulates cyclic nucleotide gated channels, which in turn control Ca influx and Ca dependent activation of chloride conductances. As a result the cilia potential becomes depolarized.
Highlights
A biochemical model is developed for the receptor, G-protein and effector (RGE) steps of olfactory signal transduction in the cilia of the vertebrate olfactory receptor neurons (ORNs)
It describes the steps from odorant binding to activation of the effector enzyme, which catalyzes the conversion of ATP to cAMP
Since our aim was to develop a model for vertebrate ORNs, certain parts of the previous model were reinterpreted
Summary
A biochemical model is developed for the receptor, G-protein and effector (RGE) steps of olfactory signal transduction in the cilia of the vertebrate olfactory receptor neurons (ORNs). Email: Geir Halnes* - geir.halnes@bt.slu.se * Corresponding author from Seventeenth Annual Computational Neuroscience Meeting: CNS*2008 Portland, OR, USA. Published: 11 July 2008 BMC Neuroscience 2008, 9(Suppl 1):O10 doi:10.1186/1471-2202-9-S1-O10 It describes the steps from odorant binding to activation of the effector enzyme, which catalyzes the conversion of ATP to cAMP.
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