Project Title

Synaptic Connectivity After Methimazole-Induced Injury

Authors' Affiliations

Lea N. Lance, Department of Biological Sciences, College of Arts and Sciences, East Tennessee State University, Johnson City, TN. Rudy T. Chapman, Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN. Diego J. Rodriguez-Gil, Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN.

Faculty Sponsor’s Department

Biomedical Sciences

Name of Project's Faculty Sponsor

Dr. Diego Rodriguez-Gil

Type

Poster: Competitive

Classification of First Author

Undergraduate Student

Project's Category

Biological Sciences

Abstract Text

Olfactory sensory neurons in the olfactory epithelium are responsible for detecting the odors we smell and are constantly dying. However, in order for the sense of smell to be maintained, the olfactory system has the unique ability to generate new neurons. After an olfactory sensory neuron is born in the olfactory epithelium, it must extend an axon towards the olfactory bulb in the central nervous system. Within the olfactory bulb, these axons make specific synaptic contacts with the dendritic processes of mitral cells, which are the main projection neurons from the olfactory bulbs into higher cortical areas in the brain. In addition to regeneration due to normal turnover, the olfactory system is also capable of recovery after an injury. The olfactory system’s ability to recover is remarkable because it is capable of regeneration after a mild injury (a portion of olfactory epithelium is removed) or a severe injury (in which the entire olfactory epithelium is removed.) A well-established model for producing a severe type of injury in the olfactory epithelium is by inducing a chemical ablation by a single injection of the drug methimazole. A specific interest in the regenerative process after injury is reestablishment of synaptic connections. We hypothesized that expression of synaptic markers will allow for establishing a timeline of functional recovery of the olfactory system after injury. Our lab has studied three synaptic vesicle associated proteins, vesicular glutamate transporter -1 (VGlut-1), vesicular glutamate transporter-2 (VGlut-2), and synaptophysin, as well as one activity-regulated protein, tyrosine hydroxylase. These studies found specific temporal expression profiles at 2, 7 and 14 days post injury. Our initial data show that VGlut-1 and VGlut-2 are decreased after injury, indicative of a reduction in synaptic connectivity in both olfactory sensory neuron axons and in dendrites of mitral cell neurons. These changes in synaptic connectivity help in understanding functional connectivity after an injury and can further be used to correlate histological axonal tracing with behavioral studies.

This document is currently not available here.

Share

COinS
 

Synaptic Connectivity After Methimazole-Induced Injury

Olfactory sensory neurons in the olfactory epithelium are responsible for detecting the odors we smell and are constantly dying. However, in order for the sense of smell to be maintained, the olfactory system has the unique ability to generate new neurons. After an olfactory sensory neuron is born in the olfactory epithelium, it must extend an axon towards the olfactory bulb in the central nervous system. Within the olfactory bulb, these axons make specific synaptic contacts with the dendritic processes of mitral cells, which are the main projection neurons from the olfactory bulbs into higher cortical areas in the brain. In addition to regeneration due to normal turnover, the olfactory system is also capable of recovery after an injury. The olfactory system’s ability to recover is remarkable because it is capable of regeneration after a mild injury (a portion of olfactory epithelium is removed) or a severe injury (in which the entire olfactory epithelium is removed.) A well-established model for producing a severe type of injury in the olfactory epithelium is by inducing a chemical ablation by a single injection of the drug methimazole. A specific interest in the regenerative process after injury is reestablishment of synaptic connections. We hypothesized that expression of synaptic markers will allow for establishing a timeline of functional recovery of the olfactory system after injury. Our lab has studied three synaptic vesicle associated proteins, vesicular glutamate transporter -1 (VGlut-1), vesicular glutamate transporter-2 (VGlut-2), and synaptophysin, as well as one activity-regulated protein, tyrosine hydroxylase. These studies found specific temporal expression profiles at 2, 7 and 14 days post injury. Our initial data show that VGlut-1 and VGlut-2 are decreased after injury, indicative of a reduction in synaptic connectivity in both olfactory sensory neuron axons and in dendrites of mitral cell neurons. These changes in synaptic connectivity help in understanding functional connectivity after an injury and can further be used to correlate histological axonal tracing with behavioral studies.