Project Title

Engulfment of Axonal Debris After Methimazole-Induced Injury

Authors' Affiliations

Rudy T. Chapman, Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN Diego J. Rodriguez-Gil, Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN

Location

BEECH MTN. ROOM 120

Start Date

4-12-2019 9:20 AM

End Date

4-12-2019 9:35 AM

Faculty Sponsor’s Department

Biomedical Sciences

Name of Project's Faculty Sponsor

Dr. Diego Rodriguez-Gil

Type

Oral Presentation

Classification of First Author

Graduate Student-Doctoral

Project's Category

Neuroscience, Polymerase Chain Reaction, Cell Biology

Abstract Text

Neurons in the olfactory epithelium that are responsible for detecting the odors we smell are constantly dying. However, the olfactory system has the unique ability to regenerate new neurons in order for the sense of smell to be maintained. After a new sensory neuron is born in the olfactory epithelium, it must extend a new axon that will travel to the olfactory bulb and make specific synaptic contact so that the odor information from the epithelium can be coded and sent to the higher cortical areas of the brain. The olfactory system’s ability to recover is also even more complex in that it is capable of regeneration after an injury in which a portion or even the entire olfactory epithelium is removed. A well established model for this type of injury in the olfactory epithelium is by inducing a chemical ablation by injection of the drug methimazole. A specific interest in the regenerative process after injury is the mechanism by which axonal debris from the dead neurons is removed. After ablation of the olfactory epithelium, the cell bodies of the neurons detach but their axons remain intact. The axonal debris must not only be removed, but must also be done so in a way that minimizes inflammation in order for new axons to be able to extend to the olfactory bulb. Axonal debris removal has been characterized both in vitro and during development. However, the mechanism of debris removal has yet to be characterized after an injury. Our lab has studied different engulfment proteins in the olfactory bulb after injury using RT-qPCR and found specific temporal expression profiles at 3, 14 and 21 days post injury. Our initial investigations involved some known engulfment proteins such as Jedi1, GULP, and Megf10. However, we found that these proteins are downregulated after an injury. Further investigation has shown that the proteins Cd11b and TLR2 are upregulated after injury. These changes in expression can begin to shed light on the mechanism of axonal debris removal after an injury and can further be used to study how inflammation is suppressed in order to allow for axon extension and synaptic contact to be reestablished.

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Apr 12th, 9:20 AM Apr 12th, 9:35 AM

Engulfment of Axonal Debris After Methimazole-Induced Injury

BEECH MTN. ROOM 120

Neurons in the olfactory epithelium that are responsible for detecting the odors we smell are constantly dying. However, the olfactory system has the unique ability to regenerate new neurons in order for the sense of smell to be maintained. After a new sensory neuron is born in the olfactory epithelium, it must extend a new axon that will travel to the olfactory bulb and make specific synaptic contact so that the odor information from the epithelium can be coded and sent to the higher cortical areas of the brain. The olfactory system’s ability to recover is also even more complex in that it is capable of regeneration after an injury in which a portion or even the entire olfactory epithelium is removed. A well established model for this type of injury in the olfactory epithelium is by inducing a chemical ablation by injection of the drug methimazole. A specific interest in the regenerative process after injury is the mechanism by which axonal debris from the dead neurons is removed. After ablation of the olfactory epithelium, the cell bodies of the neurons detach but their axons remain intact. The axonal debris must not only be removed, but must also be done so in a way that minimizes inflammation in order for new axons to be able to extend to the olfactory bulb. Axonal debris removal has been characterized both in vitro and during development. However, the mechanism of debris removal has yet to be characterized after an injury. Our lab has studied different engulfment proteins in the olfactory bulb after injury using RT-qPCR and found specific temporal expression profiles at 3, 14 and 21 days post injury. Our initial investigations involved some known engulfment proteins such as Jedi1, GULP, and Megf10. However, we found that these proteins are downregulated after an injury. Further investigation has shown that the proteins Cd11b and TLR2 are upregulated after injury. These changes in expression can begin to shed light on the mechanism of axonal debris removal after an injury and can further be used to study how inflammation is suppressed in order to allow for axon extension and synaptic contact to be reestablished.