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
N1 - Funding Information:
This work was supported by the intramural grant of RIKEN Center for Developmental Biology, the Japan Science and Technology Agency Precursory Research for Embryonic Science and Technology program, and Japan Society for the Promotion of ScienceJSPS Grants-in-Aid for Scientific Research (KAKENHI) Grants 23680038, 15H05572, 15K14336, 16K14568, and 16H06456 to T.I. The imaging experiments were supported by the RIKEN Kobe Light Microscopy Facility. Animal experiments were supported by the Laboratory for Animal Resources and Genetic Engineering at RIKEN Center for Life Science Technologies. A.M. was a RIKEN Junior Research Associate.
Funding Information:
Received August 17, 2016; accepted September 24, 2016; First published October 5, 2016. The authors declare no competing financial interests. Author contributions: K.N. and T.I. designed research; A.M. and R.I. performed research; A.T., Y.M., and T.S. contributed unpublished reagents/analytic tools; S.F. and S.A. analyzed data; A.M., K.N., and T.I. wrote the paper. This work was supported by the intramural grant of RIKEN Center for Developmental Biology, the Japan Science and Technology Agency Precursory Research for Embryonic Science and Technology program, and Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (KAKENHI) Grants 23680038, 15H05572, 15K14336, 16K14568, and 16H06456 to T.I. The imaging experiments were supported by the RIKEN Kobe Light Microscopy Facility. Animal experiments were supported by the Laboratory for Animal Resources and Genetic Engineering at RIKEN Center for Life Science Technologies. A.M. was a RIKEN Junior Research Associate. Acknowledgments: We thank M. Nomura for technical assistance; M-T Ke for microscopy; M. Leiwe for comments on the manuscript; and P. Mombaerts (OMP-GFP), J.R. Sanes (Thy1-YFP-G), and K. Svoboda (Thy1-GCaMP6f) for mouse strains. Correspondence should be addressed to Dr. Takeshi Imai, Laboratory for Sensory Circuit Formation, RIKEN Center for Developmental Biology, Chuo-ku 650-0047, Japan. E-mail: imai@cdb.riken.jp. DOI:http://dx.doi.org/10.1523/ENEURO.0242-16.2016 Copyright © 2016 Murai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
Publisher Copyright:
© 2016 Murai et al.
PY - 2016/9
Y1 - 2016/9
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.
KW - Dysosmia
KW - Glomerular map
KW - Olfactory bulb
KW - Olfactory sensory neurons
KW - Regeneration
KW - Traumatic axon Injury
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U2 - 10.1523/ENEURO.0242-16.2016
DO - 10.1523/ENEURO.0242-16.2016
M3 - Article
C2 - 27785463
AN - SCOPUS:85032144453
VL - 3
JO - eNeuro
JF - eNeuro
SN - 2373-2822
IS - 5
M1 - e0242-16.2016
ER -