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 journalArticle

2 Citations (Scopus)

Abstract

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
JournaleNeuro
Volume3
Issue number5
DOIs
Publication statusPublished - Oct 28 2016

Fingerprint

Olfactory Receptor Neurons
Olfaction Disorders
Dendrites
Axons
Wounds and Injuries
Olfactory Bulb
Smell
Automatic Data Processing

Cite this

Distorted Coarse Axon Targeting and Reduced Dendrite Connectivity Underlie Dysosmia after Olfactory Axon Injury. / Murai, Aya; Iwata, Ryo; Fujimoto, Satoshi; Aihara, Shuhei; Tsuboi, Akio; Muroyama, Yuko; Saito, Tetsuichiro; Nishizaki, Kazunori; Imai, Takeshi.

In: eNeuro, Vol. 3, No. 5, 28.10.2016.

Research output: Contribution to journalArticle

Murai, Aya ; Iwata, Ryo ; Fujimoto, Satoshi ; Aihara, Shuhei ; Tsuboi, Akio ; Muroyama, Yuko ; Saito, Tetsuichiro ; Nishizaki, Kazunori ; Imai, Takeshi. / Distorted Coarse Axon Targeting and Reduced Dendrite Connectivity Underlie Dysosmia after Olfactory Axon Injury. In: eNeuro. 2016 ; Vol. 3, No. 5.
@article{21f2251fec94479899833e4193d18043,
title = "Distorted Coarse Axon Targeting and Reduced Dendrite Connectivity Underlie Dysosmia after Olfactory Axon Injury",
abstract = "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.",
author = "Aya Murai and Ryo Iwata and Satoshi Fujimoto and Shuhei Aihara and Akio Tsuboi and Yuko Muroyama and Tetsuichiro Saito and Kazunori Nishizaki and Takeshi Imai",
year = "2016",
month = "10",
day = "28",
doi = "10.1523/ENEURO.0242-16.2016",
language = "English",
volume = "3",
journal = "eNeuro",
issn = "2373-2822",
publisher = "Society for Neuroscience",
number = "5",

}

TY - JOUR

T1 - Distorted Coarse Axon Targeting and Reduced Dendrite Connectivity Underlie Dysosmia after Olfactory Axon Injury

AU - Murai, Aya

AU - Iwata, Ryo

AU - Fujimoto, Satoshi

AU - Aihara, Shuhei

AU - Tsuboi, Akio

AU - Muroyama, Yuko

AU - Saito, Tetsuichiro

AU - Nishizaki, Kazunori

AU - Imai, Takeshi

PY - 2016/10/28

Y1 - 2016/10/28

N2 - 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.

AB - 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.

U2 - 10.1523/ENEURO.0242-16.2016

DO - 10.1523/ENEURO.0242-16.2016

M3 - Article

VL - 3

JO - eNeuro

JF - eNeuro

SN - 2373-2822

IS - 5

ER -