Distorted coarse axon targeting and reduced dendrite connectivity underlie Dysosmia after olfactory axon injury

Aya Murai, Ryo Iwata, Satoshi Fujimoto, Shuhei Aihara, Akio Tsuboi, Yuko Muroyama, Tetsuichiro Saito, Kazunori Nishizaki, Takeshi Imai

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


The glomerular map in the olfactory bulb (OB) is the basis for odor recognition. Once established during development, the glomerular map is stably maintained throughout the life of an animal despite the continuous turnover of olfactory sensory neurons (OSNs). However, traumatic damage to OSN axons in the adult often leads to dysosmia, a qualitative and quantitative change in olfaction in humans. A mouse model of dysosmia has previously indicated that there is an altered glomerular map in the OB after the OSN axon injury; however, the underlying mechanisms that cause the map distortion remain unknown. In this study, we examined how the glomerular map is disturbed and how the odor information processing in the OB is affected in the dysosmia model mice. We found that the anterior-posterior coarse targeting of OSN axons is disrupted after OSN axon injury, while the local axon sorting mechanisms remained. We also found that the connectivity of mitral/tufted cell dendrites is reduced after injury, leading to attenuated odor responses in mitral/tufted cells. These results suggest that existing OSN axons are an essential scaffold for maintaining the integrity of the olfactory circuit, both OSN axons and mitral/tufted cell dendrites, in the adult.

Original languageEnglish
Article numbere0242-16.2016
Issue number5
Publication statusPublished - Sept 2016


  • Dysosmia
  • Glomerular map
  • Olfactory bulb
  • Olfactory sensory neurons
  • Regeneration
  • Traumatic axon Injury

ASJC Scopus subject areas

  • General Neuroscience


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