Title

Neuronal Response to and Potential Role of Chondroitin Sulfate in Astrogliosis

Presenter Information

Ann Harper, Murray State University

Major

Biology

List all Project Mentors & Advisor(s)

Dr. David Canning

Presentation Format

Event

Abstract/Description

Brain trauma and neurodegenerative diseases are the basis for much of the research being conducted today. When trauma is induced to the brain, an inflammatory response takes place termed gliosis. Gliosis was mimicked in vitro using astrocytes extracted from P1 rat pups cultured with beta amyloid protein. Culture matrices were conditioned with an in vitro astrocytic response to beta amyloid protein. With TRITC labeling, deposition of chondroitin sulfate from the astrocytes during their reaction to beta amyloid was demonstrated. Neurite outgrowth was tested by replacing astrocytes with retinal ganglia cells dissected from 6-day chick embryos. The final step of measuring neurite outgrowth of the retinal ganglia cells was accomplished by obtaining photomicrographs of the cells after culturing for various lengths of time. Our data shows evidence that the deposition of chondroitin sulfate by the astrocytic response was inhibitory to neurite outgrowth. Beta amyloid protein, thought to be an inhibitor to neurite outgrowth, had no effect on neurite outgrowth while those matrices conditioned by astrocytes depositing chondroitin sulfate showed significant inhibition to neurite outgrowth.

Other Affiliations

Science and Mathematics

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Neuronal Response to and Potential Role of Chondroitin Sulfate in Astrogliosis

Brain trauma and neurodegenerative diseases are the basis for much of the research being conducted today. When trauma is induced to the brain, an inflammatory response takes place termed gliosis. Gliosis was mimicked in vitro using astrocytes extracted from P1 rat pups cultured with beta amyloid protein. Culture matrices were conditioned with an in vitro astrocytic response to beta amyloid protein. With TRITC labeling, deposition of chondroitin sulfate from the astrocytes during their reaction to beta amyloid was demonstrated. Neurite outgrowth was tested by replacing astrocytes with retinal ganglia cells dissected from 6-day chick embryos. The final step of measuring neurite outgrowth of the retinal ganglia cells was accomplished by obtaining photomicrographs of the cells after culturing for various lengths of time. Our data shows evidence that the deposition of chondroitin sulfate by the astrocytic response was inhibitory to neurite outgrowth. Beta amyloid protein, thought to be an inhibitor to neurite outgrowth, had no effect on neurite outgrowth while those matrices conditioned by astrocytes depositing chondroitin sulfate showed significant inhibition to neurite outgrowth.