Location
Additional Presentations- College of Science and Mathematics
Document Type and Release Option
Thesis Presentation (Restricted to Georgia Southern)
Faculty Mentor
Dr. Sarah Rotschafer
Faculty Mentor Email
.
Presentation Year
2021
Start Date
26-4-2021 12:00 AM
End Date
30-4-2021 12:00 AM
Keywords
Georgia Southern University, Honors Symposium, Presentation
Description
Fragile X syndrome (FXS) is the most common single genetic cause of autism. In FXS, the Fmr1 gene is transcriptionally silenced preventing the formation of fragile X mental retardation protein (FMRP). Individuals with FXS show hypersensitivity to auditory stimuli. Fmr1 knockout mice replicate many symptoms seen in individuals with FXS including heightened auditory responsiveness. Previous studies using Fmr1 knockout mice demonstrate imbalances in inhibitory and excitatory inputs within auditory brain stem nuclei as well as altered astrocyte expression. In particular, the lateral superior olivary nucleus (LSO) shows an imbalance in synaptic inputs and an increased number of astrocytes. Astrocyte dysfunction may be impactful because astrocytes regulate synaptic development and synaptic pruning. Astrocytes also act as an intermediary between neurons and blood vessels in the brain. The current study was conducted to determine if the increase in astrocytes is associated with excessive vascularization within the LSO. Blood vessels in brain sections from wild-type and Fmr1 knockout mice were labeled using isolectin, and fluorescent imaging was performed. ImageJ software will be used to determine the density of blood vessels in wild type vs knockout mice LSO. It is expected that Fmr1 knockout mice will exhibit a higher density of blood vessels.
Academic Unit
College of Science and Mathematics
Vascularization of LSO in Fragile X Model Mice
Additional Presentations- College of Science and Mathematics
Fragile X syndrome (FXS) is the most common single genetic cause of autism. In FXS, the Fmr1 gene is transcriptionally silenced preventing the formation of fragile X mental retardation protein (FMRP). Individuals with FXS show hypersensitivity to auditory stimuli. Fmr1 knockout mice replicate many symptoms seen in individuals with FXS including heightened auditory responsiveness. Previous studies using Fmr1 knockout mice demonstrate imbalances in inhibitory and excitatory inputs within auditory brain stem nuclei as well as altered astrocyte expression. In particular, the lateral superior olivary nucleus (LSO) shows an imbalance in synaptic inputs and an increased number of astrocytes. Astrocyte dysfunction may be impactful because astrocytes regulate synaptic development and synaptic pruning. Astrocytes also act as an intermediary between neurons and blood vessels in the brain. The current study was conducted to determine if the increase in astrocytes is associated with excessive vascularization within the LSO. Blood vessels in brain sections from wild-type and Fmr1 knockout mice were labeled using isolectin, and fluorescent imaging was performed. ImageJ software will be used to determine the density of blood vessels in wild type vs knockout mice LSO. It is expected that Fmr1 knockout mice will exhibit a higher density of blood vessels.
Comments
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