RT Journal Article
SR Electronic
T1 Distorted Coarse Axon Targeting and Reduced Dendrite Connectivity Underlie Dysosmia after Olfactory Axon Injury
JF eneuro
JO eNeuro
FD Society for Neuroscience
SP ENEURO.0242-16.2016
DO 10.1523/ENEURO.0242-16.2016
VO 3
IS 5
A1 Aya Murai
A1 Ryo Iwata
A1 Satoshi Fujimoto
A1 Shuhei Aihara
A1 Akio Tsuboi
A1 Yuko Muroyama
A1 Tetsuichiro Saito
A1 Kazunori Nishizaki
A1 Takeshi Imai
YR 2016
UL http://www.eneuro.org/content/3/5/ENEURO.0242-16.2016.abstract
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.