Date of Presentation
5-2-2024 12:00 AM
College
Rowan-Virtua School of Osteopathic Medicine
Poster Abstract
Many neurotropic viruses cause more significant pathology in younger hosts as their brains are still developing. This experiment asked how central nervous system (CNS) viral-infections affect the development of synapses in the pediatric brain during infection and post-infection. Synaptogenesis is at its peak in pediatric mice (10 days old) and we hypothesized that a neurotropic infection could disrupt synaptic proteins. We used a transgenic mouse model where measles virus (MV) infects only mature neurons, leading us to question whether synapses were impacted. We examined synaptic markers in the cerebellum and hippocampus in MV-infected and uninfected mice 9 days and 90 days post-infection through western blot analysis. We found differential downregulation of pre-synaptic proteins (synapsins 1, 2 and 3) during infection, which was dependent on the brain region and the time point examined. This highlights the short and long-term consequences of a pediatric infection on neurodevelopment and potential dysregulation of synaptogenesis.
Keywords
Brain, neurology, pediatrics, synapses, mouse model, brain development, neurodevelopment
Disciplines
Developmental Neuroscience | Disease Modeling | Medical Neurobiology | Medicine and Health Sciences | Nervous System | Nervous System Diseases | Neurosciences | Virus Diseases
Document Type
Poster
DOI
10.31986/issn.2689-0690_rdw.stratford_research_day.173_2024
Included in
Developmental Neuroscience Commons, Disease Modeling Commons, Medical Neurobiology Commons, Nervous System Commons, Nervous System Diseases Commons, Neurosciences Commons, Virus Diseases Commons
Pediatric Neurotropic Infection Alters Synaptic Development in the Developing Brain
Many neurotropic viruses cause more significant pathology in younger hosts as their brains are still developing. This experiment asked how central nervous system (CNS) viral-infections affect the development of synapses in the pediatric brain during infection and post-infection. Synaptogenesis is at its peak in pediatric mice (10 days old) and we hypothesized that a neurotropic infection could disrupt synaptic proteins. We used a transgenic mouse model where measles virus (MV) infects only mature neurons, leading us to question whether synapses were impacted. We examined synaptic markers in the cerebellum and hippocampus in MV-infected and uninfected mice 9 days and 90 days post-infection through western blot analysis. We found differential downregulation of pre-synaptic proteins (synapsins 1, 2 and 3) during infection, which was dependent on the brain region and the time point examined. This highlights the short and long-term consequences of a pediatric infection on neurodevelopment and potential dysregulation of synaptogenesis.