Open AccessCross‐talk between olfactory second messenger pathways
Author(s) -
Vogl Alexander,
Noé Johannes,
Breer Heinz,
Boekhoff Ingrid
Publication year - 2000
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1046/j.1432-1327.2000.01503.x
Subject(s) - second messenger system , odor , signal transduction , olfactory system , biology , cyclase , olfaction , phospholipase c , long term potentiation , antagonism , protein kinase a , stimulation , endocrinology , microbiology and biotechnology , chemistry , biochemistry , receptor , neuroscience , kinase
The second messengers 3′‐5′‐cyclic‐monophosphate (cAMP) and inositol 1,4,5‐trisphosphate (Ins P 3 ) have been implicated in olfactory signal transduction in various species. The results of the present study provide evidence that the two olfactory second messenger pathways in rat olfactory neurons do not work independently but rather show a functional antagonism: whereas inhibition of phospholipase C (PLC) in isolated olfactory cilia by U‐73122 led to an augmentation of odor‐induced cAMP signaling, activation of the phosphoinositol pathway resulted in attenuation of odor‐induced cAMP formation. Furthermore, this study indicates that elevated cAMP levels cause suppression of odor‐induced Ins P 3 signaling, whereas inhibition of adenylate cyclase (AC) by cis N ‐(2‐phenylcyclopentyl)azacylotridec‐1‐en‐2‐amine (MDL‐12,330 A) results in potentiation of odor‐induced Ins P 3 formation. Concerning the molecular mechanism involved in cross‐interaction, the experimental data indicate that the observed antagonism of elevated cAMP is based on inhibition of PLC activation rather than on stimulation of Ins P 3 degradation. As blockage of the endogenous protein kinase A (PKA) prevented the inhibitory effect of cAMP, the suppression of odor‐induced Ins P 3 signaling by cAMP may be mediated by a PKA‐controlled reaction.