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Odorant Stimulation Promotes Survival of Rodent Olfactory Receptor Neurons via PI3K/Akt Activation and Bcl-2 Expression

Odorant Stimulation Promotes Survival of Rodent Olfactory Receptor Neurons via PI3K/Akt Activation and Bcl-2 Expression
Kim, SY[Kim, So Yeun]Yoo, SJ[Yoo, Seung-Jun]Ronnett, GV[Ronnett, Gabriele V.]Kim, EK[Kim, Eun-Kyoung]Moon, C[Moon, Cheil]
DGIST Authors
Kim, SY[Kim, So Yeun]; Yoo, SJ[Yoo, Seung-Jun]; Ronnett, GV[Ronnett, Gabriele V.]; Kim, EK[Kim, Eun-Kyoung]Moon, C[Moon, Cheil]
Issue Date
Molecules and Cells, 38(6), 535-539
Article Type
2 Morpholino 8 PhenylchromoneAdultAnimal CellAnimal ExperimentBcl-2Cell SurvivalControlled StudyDissociated Cell CultureEnzyme ActivationIn Vitro StudyIn Vivo StudyMaleMessenger RNAMouseNon-HumanNorthern BlottingOdorOdorantOlfactory ReceptorOlfactory Receptor NeuronOlfactory SystemPhosphatidylinositol 3 KinasePI3K/AktProtein BCL 2Protein ExpressionProtein Kinase BRatSensory StimulationSignal TransductionSmall Interfering RnaSurvivalUpregulation
Olfactory stimulation activates multiple signaling cascades in order to mediate activity-driven changes in gene expression that promote neuronal survival. To date, the mechanisms involved in activity-dependent olfactory neuronal survival have yet to be fully elucidated. In the current study, we observed that olfactory sensory stimulation, which caused neuronal activation, promoted activation of the phosphatidylinositol 3’-kinase (PI3K)/Akt pathway and the expression of Bcl-2, which were responsible for olfactory receptor neuron (ORN) survival. We demonstrated that Bcl-2 expression increased after odorant stimulation both in vivo and in vitro. We also showed that odorant stimulation activated Akt, and that Akt activation was completely blocked by incubation with both a PI3K inhibitor (LY294002) and Akt1 small interfering RNA. Moreover, blocking the PI3K/Akt pathway diminished the odorantinduced Bcl-2 expression, as well as the effects on odorant-induced ORN survival. A temporal difference was noted between the activation of Akt1 and the expression of Bcl-2 following odorant stimulation. Blocking the PI3K/Akt pathway did not affect ORN survival in the time range prior to the increase in Bcl-2 expression, implying that these two events, activation of the PI3K pathway and Bcl-2 induction, were tightly connected to promote post-translational ORN survival. Collectively, our results indicated that olfactory activity activated PI3K/Akt, induced Bcl-2, and promoted long term ORN survival as a result. © The Korean Society for Molecular and Cellular Biology. All rights reserved.
Korean Society for Molecular and Cellular Biology
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Brain and Cognitive SciencesLab of Neuro-Metabolism & Neurometabolomic Research Center1. Journal Articles

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