Role of NPY in neuroregeneration following Satratoxin G induced injury in the mouse olfactory epithelium
VanGelderen, Caitlyn Q.
MetadataShow full item record
The human olfactory epithelium (OE) contains olfactory sensory neurons (OSNs) which detect airborne compounds and send signals through to the olfactory bulb. What is unique about this system is that the epithelium undergoes continuous regeneration throughout life. When an OSN becomes injured, it releases ATP which binds to microvillous cells. This binding causes a cascade that triggers the release of neuropeptide Y (NPY); NPY binds to basal “stem” cells that proliferate into new OSNs. One airborne toxicant that induces injury of OSNs is Satratoxin G (SG) which is found in spores of Stachybotrys chartarum, a black mold found in water-damaged homes. The aim of this study was to determine if daily treatments with NPY after a single aspiration of SG could protect against toxicant’s damaging effects. Male mice were anesthetized and intranasally aspired with a saline control solution or SG solution. For six successive days following initial treatment, mice aspired NPY solution or saline control solution. Mice received injections of BrdU which becomes incorporated into DNA during proliferation of the basal cells. Tissue slices of the OE were taken and measurements were taken to determine thickness of the epithelium in 3 locations of the OE. BrdU incorporation was analyzed to measure basal cell proliferation. SG exposure significantly reduced epithelial thickness in the ecto-turbinates II and endo-turbinates 2 but not in the septum. SG also significantly increased levels of proliferation of basal cells. Treatment with NPY did not protect against SG-induced cell death or reduction of epithelial thickness in the olfactory epithelium. Further research into the proliferation mechanism after SG exposure is needed to develop respiratory treatments for people living in S. chartarum contaminated homes.