PT  - JOURNAL ARTICLE
AU  - Jordan N. Norwood
AU  - Akshay P. Gharpure
AU  - Raju Kumal
AU  - Kevin L. Turner
AU  - Lauren Ferrer Pistone
AU  - Randy Vander Wal
AU  - Patrick J. Drew
TI  - Intranasal Administration of Functionalized Soot Particles Disrupts Olfactory Sensory Neuron Progenitor Cells in the Neuroepithelium
AID  - 10.1101/2020.08.19.256297
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.08.19.256297
4099  - http://biorxiv.org/content/early/2020/08/19/2020.08.19.256297.short
4100  - http://biorxiv.org/content/early/2020/08/19/2020.08.19.256297.full
AB  - Exposure to air pollution has been linked to the development of neurodegenerative diseases and anosmia, but the underlying mechanism is not known. Additionally, the loss of olfactory function often precedes the onset of neurodegenerative diseases. Chemical ablation of olfactory sensory neurons blocks the drainage of cerebrospinal fluid (CSF) through the cribriform plate and alters normal CSF production and/or circulation. Damage to this drainage pathway could contribute to the development of neurodegenerative diseases and could link olfactory sensory neuron health and neurodegeneration. Here, we investigated the impact of intranasal treatment of combustion products (laboratory-generated soots) and their oxygen functionalized derivatives on mouse olfactory sensory neurons, olfactory nerve cell progenitors, and the behavior of the mouse. We found that after a month of every-other-day intranasal treatment of soots, there was minimal effect on olfactory sensory neuron anatomy or exploratory behavior in the mouse. However, oxygen-functionalized soot caused a large decrease in globose basal cells, which are olfactory progenitor cells. These results suggest that exposure to air pollution damages the olfactory neuron progenitor cells, and could lead to decreases in the number of olfactory neurons, potentially disrupting CSF drainage.Competing Interest StatementThe authors have declared no competing interest.