Presentation Title

Vascularization of LSO in Fragile X Model Mice

Faculty Mentor

Dr. Sarah Rotschafer, Dr. Robert Mans

Faculty Mentor Email

rotschafer_se@mercer.edu, rmans@georgiasouthern.edu

Presentation Type and Release Option

Research Poster Presentation with Supplemental Video (File Not Available for Download)

Location

COUR Symposium 2021

Presentation Year

2021

Start Date

4-19-2021 12:00 AM

End Date

April 2021

Abstract

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 (Fmr1 KO) 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), a nucleus in the auditory brainstem, shows altered synaptic inputs and an increased in the number of astrocytes expressed. 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 was 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

Department of Biology

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Apr 19th, 12:00 AM Apr 20th, 12:00 AM

Vascularization of LSO in Fragile X Model Mice

COUR Symposium 2021

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 (Fmr1 KO) 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), a nucleus in the auditory brainstem, shows altered synaptic inputs and an increased in the number of astrocytes expressed. 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 was 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.