Biology Project Abstract
CHANGES IN GLUTAMATE TRANSPORTER EXPRESSION FOLLOWING LIGHT DAMAGE TO MOUSE RETINA (2002)
Presenter:
Neelima Vidula, Illinois Mathematics and Science Academy, 1500 West Sullivan Road, Aurora, IL 60506; vneelima@imsa.edu
Mentors:
Dr. Vijay Sarthy, Northwestern University Medical School, 2160 South First Avenue, Chicago, IL 60611
V. Joseph Dudley, M.S., Northwestern University Medical School, Department of Ophthalmology, 300 East Superior St., Chicago, IL 60611
Abstract:
Glutamate, a neurotransmitter, is known to play a role in numerous diseases of the central nervous system. High concentrations of glutamate can also damage the mammalian retina leading to eye disorders such as glaucoma. GLAST, a glutamate transporter, may prevent detrimental glutamate levels by controlling the uptake of excess glutamate. The purpose of this research was to elucidate the relationship between glutamate levels and retinal damage induced by long-term light exposure. After exposing BALB/c albino mice to constant light for 2 to 8 weeks, their retinas were isolated and the total RNA was extracted and reverse transcribed. PCR experiments were conducted using primers against GLAST. Cryostat sectioning was performed on frozen retinas to visualize the light damage to the photoreceptor layer of the mouse retina. Antibodies against GLAST and another glutamate transporter, GFAP, were used to detect the presence of proteins in the retina. PCR results indicated that GLAST mRNA levels decreased rapidly between 2 to 4 weeks of light damage, and by 10 weeks, there is little detectable mRNA. These data suggest that a decrease in GLAST mRNA over time may result in excess glutamate and contribute to the retinal damage.