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. 2010 Jun 2;35(7):533–539. doi: 10.1093/chemse/bjq045

Figure 2.

Figure 2

Potential model for phosphoinositide-3-kinase (PI3K)-dependent opponent input to rodent olfactory receptor neurons (ORNs). One component of a binary odorant mixture (yellow circles) excites the cell through the canonical cyclic nucleotide signaling pathway: the olfactory receptor (OR) activates a G-protein (Gαolf), which in turn activates adenylyl cyclase (AC3) to produce cyclic adenosine monophosphate (cAMP) that activates the olfactory cyclic nucleotide gated channel (CNGC). The other component (blue stars), potentially binding to the same OR, inhibits the cell by activating phosphoinositide 3-kinase (PI3K) through the beta/gamma subunit of the same or still unknown G-protein. Activation of PI3K produces phosphatidylinositol (3,4,5) trisphosphate (PIP3), which negatively regulates sensitivity of the CNGC to cAMP and reduces the net output of the ORN. The involvement of phospholipase C (PLC, faded) to produce inositol-1,4,5-phosphate (IP3) and diacylglycerol (DAG) remains to be explored.