SPLTRAK Abstract Submission
Methimazole-Induced Injury Alters Levels of Expression of Engulfment Proteins
Rudy T. Chapman & Diego J. Rodriguez-Gil
East Tennessee State University, Johnson City, TN, United States

The olfactory system has the unique ability to regenerate throughout life, which allows the sense of smell to be maintained in spite of the high death rate of olfactory sensory neurons. When a sensory neuron from the olfactory epithelium dies, another sensory neuron is born to take its place and extends an axon to establish synaptic contact in the olfactory bulb. In addition to regeneration due to normal turnover, the olfactory system is also able to regenerate after an injury in which a portion or even the entire olfactory epithelium is removed. An established model of injury to the olfactory system is by chemical ablation through an acute injection of the drug methimazole. An element of regeneration after an injury that is of interest is the mechanism by which cellular debris from ablated neurons is removed. When the olfactory epithelium is removed due to an injury, the cell bodies of the neurons in the epithelium are removed but their axons remain. The axonal debris from the ablated neurons must be removed in a way that minimizes inflammation in order to allow for extension of new axons to the olfactory bulb. In vitro and during development this role has been attributed to the olfactory ensheathing cells, yet what happens after injury or the mechanism involved in the process have not been identified. In order to understand how cellular debris is removed after injury, our lab has studied the engulfment proteins Jedi1, Gulp1, and Megf10 using RT-qPCR. We found specific temporal expression profiles from olfactory bulbs at 3, 14, and 21 days post injury that start to shed a light into the role of these proteins in the engulfment process. Changes in expression of engulfment proteins after injury will help in understanding the mechanisms by which neuronal debris is cleared after an injury.