Visual Abstract
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.
Footnotes
The authors declare no competing financial interests.
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.
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