Phosphoinositide and Erk signaling pathways mediate activity-driven rodent olfactory sensory neuronal survival and stress mitigation

So Yeun Kim, Alex Mammen, Seung Jun Yoo, Bongki Cho, Eun Kyoung Kim, Jong In Park, Cheil Moon, Gabriele V. Ronnett

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Olfactory sensory neurons (OSNs) are the initial site for olfactory signal transduction. Therefore, their survival is essential to olfactory function. In the current study, we demonstrated that while odorant stimulation promoted rodent OSN survival, it induced generation of reactive oxygen species in a dose- and time-dependent manner as well as loss of membrane potential and fragmentation of mitochondria. The MEK-Erk pathway played a critical role in mediating these events, as its inhibition decreased odorant stimulation-dependent OSN survival and exacerbated intracellular stress measured by reactive oxygen species generation and heat-shock protein 70 expression. The phosphoinositide pathway, rather than the cyclic AMP pathway, mediated the odorant-induced activation of the MEK-Erk pathway. These findings provide important insights into the mechanisms of activity-driven OSN survival, the role of the phosphoinositide pathway in odorant signaling, and demonstrate that odorant detection and odorant stimulation-mediated survival proceed via independent signaling pathways. This mechanism, which permits independent regulation of odorant detection from survival signaling, may be advantageous if not diminished by repeated or prolonged odor exposure.

Original languageEnglish (US)
Pages (from-to)486-498
Number of pages13
JournalJournal of Neurochemistry
Issue number3
StatePublished - Aug 1 2015


  • activity-driven survival
  • mitogen-activated protein kinase
  • olfactory
  • oxidative stress
  • phosphoinositide
  • sensory transduction

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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