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Published on: June 5, 2017
Distorted Coarse Axon Targeting and Reduced Dendrite Connectivity Underlie Dysosmia after Olfactory Axon Injury
Aya Murai1, Ryo Iwata2, Satoshi Fujimoto2
1Laboratory for Sensory Circuit Formation, RIKEN Center for Developmental Biology, Chuo-ku 650-0047, Japan; Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Olfactory sensory neuron axon injury disrupts the olfactory bulb map, impairing odor recognition. Existing axons act as a crucial scaffold for maintaining the olfactory circuit
Area of Science:
- Neuroscience
- Olfactory System Biology
- Sensory Neuroscience
Background:
- The glomerular map in the olfactory bulb (OB) is critical for odor recognition and is generally stable despite olfactory sensory neuron (OSN) turnover.
- Traumatic injury to adult OSN axons can cause dysosmia, altering olfaction, but the mechanisms behind OB map distortion remain unclear.
Purpose of the Study:
- To investigate how OSN axon injury disturbs the glomerular map and affects odor information processing in the OB.
- To elucidate the mechanisms underlying OB map distortion following adult OSN axon injury.
Main Methods:
- Utilized a mouse model of dysosmia to study OB map alterations after OSN axon injury.
- Examined OSN axon targeting and mitral/tufted cell dendritic connectivity post-injury.
Main Results:
- OSN axon injury disrupted anterior-posterior coarse targeting within the OB, while local sorting mechanisms remained intact.
- Mitral/tufted cell dendritic connectivity was reduced post-injury, leading to diminished odor responses.
- These findings indicate that existing OSN axons are essential for maintaining the adult olfactory circuit's integrity.
Conclusions:
- The integrity of the olfactory circuit, including both OSN axons and mitral/tufted cell dendrites, relies on existing OSN axons as a scaffold in the adult.
- OSN axon injury leads to significant disruptions in OB organization and function, contributing to olfactory deficits.
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