Neuroplastic changes in the olfactory bulb associated with nasal inflammation in mice

Publication date: Available online 10 October 2018

Source: Journal of Allergy and Clinical Immunology

Author(s): Sanae Hasegawa-Ishii, Atsuyoshi Shimada, Fumiaki Imamura

Abstract

Background

Rhinitis and rhinosinusitis are olfactory disorders caused by inflammation of the nasal passage and paranasal sinuses. Although chronic rhinosinusitis patients have smaller olfactory bulbs (OBs), there is limited knowledge regarding the influence of chronic nasal inflammation on OB neurons.

Objective

Repeated intranasal administration of lipopolysaccharide (LPS) that induced persistent nasal inflammation in mice caused a loss of olfactory sensory neurons (OSNs) and gliosis and synaptic loss in the OB within three weeks. The present study aimed to clarify the effects of long-term LPS treatment on the OB neurocircuit.

Methods

LPS was repeatedly administered into a mouse nostril for up to 24 weeks. For the recovery analyses, the mice received LPS for 10 weeks and were subsequently maintained without additional treatment for another 10 weeks. The effects of these treatments on the OB were histologically examined. Three or more mice were analyzed per group.

Results

Long-term repeated LPS administration caused OB atrophy, particularly in the layers along which OSN axons travel and in the superficial external plexiform layer (sEPL), in which tufted cells form synapses with interneurons. Interestingly, the OB recovered from atrophy following the cessation of LPS administration: the OB volume and sEPL thickness returned to the pretreatment level after the nontreatment period. In contrast, the regeneration of OSN was incomplete.

Conclusion

These results suggest that chronic nasal inflammation induces structural changes in a specific OB circuit related to tufted cells, while tufted cells retain a high degree of plasticity that enables recovery from structural damages after inflammation subsides.

Graphical abstract

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