Event Title
Quantifying Cochlear Nerve Myelination in Mice Lacking Thyroid Hormone Transporters
Location
CSU Ballroom
Start Date
10-4-2018 10:00 AM
End Date
10-4-2018 11:30 AM
Student's Major
Biological Sciences
Student's College
Science, Engineering and Technology
Mentor's Name
David Sharlin
Mentor's Department
Biological Sciences
Mentor's College
Science, Engineering and Technology
Description
Thyroid hormone (TH) is essential for development of many organs and tissues, especially nervous tissue. Without access to TH, the architecture of neuronal tissue develops improperly, leading to functional deficits in neurons. One disease where this is the case is Allen-Herndon-Dudley Syndrome (AHDS), which is caused by mutations in the MCT8 gene. MCT8 mutations lead to severe psychomotor retardation, with global developmental delays and severe intellectual disabilities. Mice lacking two TH transporters - Mct8 and Oatp1c1 - that facilitate TH uptake and efflux across the cell membrane, model AHDS. Recently, we found that mice lacking both transporters have normal cochlear development, but display delayed auditory signaling. Thus, our experiments aim to test the hypothesis that auditory deficits observed in mice lacking Mct8 and Oatp1c1 is due, in part, to altered myelination of the auditory pathway. Our previous work using FluroMyelin staining revealed decreases in myelin throughout the cochlea in double knockout mice. However, to quantitate myelin changes, we are using qRT-PCR to directly measure myelin associated glycoprotein (MAG) mRNA levels in cochlear and peripheral nervous tissues. Based on our Fluoromyelin observation, we expect to observe decreased MAG mRNA within the cochlea, supporting our original hypothesis. Overall, this research will further define the need for TH transporters in development of normal auditory function. Understanding the mechanism involved in this process may help those who suffer from AHDS, leading to a better quality of life for these individuals and many others who also have auditory deficits due to low TH.
Quantifying Cochlear Nerve Myelination in Mice Lacking Thyroid Hormone Transporters
CSU Ballroom
Thyroid hormone (TH) is essential for development of many organs and tissues, especially nervous tissue. Without access to TH, the architecture of neuronal tissue develops improperly, leading to functional deficits in neurons. One disease where this is the case is Allen-Herndon-Dudley Syndrome (AHDS), which is caused by mutations in the MCT8 gene. MCT8 mutations lead to severe psychomotor retardation, with global developmental delays and severe intellectual disabilities. Mice lacking two TH transporters - Mct8 and Oatp1c1 - that facilitate TH uptake and efflux across the cell membrane, model AHDS. Recently, we found that mice lacking both transporters have normal cochlear development, but display delayed auditory signaling. Thus, our experiments aim to test the hypothesis that auditory deficits observed in mice lacking Mct8 and Oatp1c1 is due, in part, to altered myelination of the auditory pathway. Our previous work using FluroMyelin staining revealed decreases in myelin throughout the cochlea in double knockout mice. However, to quantitate myelin changes, we are using qRT-PCR to directly measure myelin associated glycoprotein (MAG) mRNA levels in cochlear and peripheral nervous tissues. Based on our Fluoromyelin observation, we expect to observe decreased MAG mRNA within the cochlea, supporting our original hypothesis. Overall, this research will further define the need for TH transporters in development of normal auditory function. Understanding the mechanism involved in this process may help those who suffer from AHDS, leading to a better quality of life for these individuals and many others who also have auditory deficits due to low TH.
Recommended Citation
Peterson, Stephanie and Marissa Swenson. "Quantifying Cochlear Nerve Myelination in Mice Lacking Thyroid Hormone Transporters." Undergraduate Research Symposium, Mankato, MN, April 10, 2018.
https://cornerstone.lib.mnsu.edu/urs/2018/poster-session-A/17
