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 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/early/2016/10/05/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 human. 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.Significance Statement: Olfactory sensory neurons (OSNs) have a unique ability to regenerate throughout the life of animals. Therefore, OSNs are newly generated and project to the olfactory bulb (OB) even after injury. However, it has been known that severe head trauma, which accompanies the transection of OSN axons, often leads to dysosmia (qualitative and quantitative changes in olfaction). Currently there is no effective therapy for dysosmia patients. To gain mechanistic insights, we investigated the anatomical and functional changes of the olfactory system after OSN axon injury, and found defects in coarse OSN axon targeting and dendrite connectivity of mitral cells. Based on these findings, possible future strategies for dysosmia will be discussed.