Abstract # 2045 Nasal inflammatory stage-associated plastic changes in the olfactory bulb neurocircuit

Abstract

We are exposed to harmful environmental agents that may cause nasal inflammation. Although prolonged nasal inflammation results in long-lasting olfactory loss, little is known about the influence of chronic nasal inflammation on the olfactory bulb (OB). We made a mouse model of chronic nasal inflammation by repeatedly administering lipopolysaccharide (LPS) to nostril and histologically analyzed changes in the olfactory epithelium (OE) and OB. Mice received LPS or saline every other day (3 times per week) for 3, 10, 18 or 24 weeks. For the recovery analyses, the mice treated with LPS for 10 weeks were housed without treatment for another 10 weeks. LPS induced OE inflammation with a loss of olfactory sensory neurons (OSNs). More than 10 weeks of LPS administration caused robust OB atrophy with a complete loss of OSNs. In atrophied OB, a prominent shrinkage occurred in the external plexiform layer (EPL) in addition to the olfactory nerve and glomerular layers. The superficial layer of the EPL, in which tufted cells form dendrodendritic synapses with interneurons, underwent shrinkage in a selective manner, although neither tufted cells nor interneurons underwent cell death. The atrophied OB returned to the normal size after the 10-week period of no treatment. These indicate a particular OB circuit, in which tufted cells are involved, is vulnerable to a chronic nasal inflammation but retains high plasticity to recover from atrophy.