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Characterization of a Neuroprotective Retinal Synapse After Inducing Glaucoma in Long Evans Rats

Faculty Mentor

Dr. Cindy Linn

Department

Biological Sciences

Presentation Date

4-13-2017

Document Type

Poster

Abstract

Glaucoma is a group of degenerative retinal diseases characterized by progressive loss of retinal ganglion cells (RGCs) and their axons leading to irreversible loss of vision. Neuroprotection has been defined as any intervention that prevents optic nerve damage or RGC death. The neurotransmitter, acetycholine (ACh), has been linked to neuroprotection against excitotoxic cell death and neurodegenerative diseases of the central nervous system (CNS). Results from our lab have demonstrated that ACh provides neuroprotection against glutamate-induced excitotoxicity in isolated pig and rat RGCs in vitro. Additional studies using an in vivo rat model of glaucoma have shown that intravitreal injections or eye drop application of the a7 nAChR selective agonist, PNU-282987, triggers neuroprotection against the normal loss of RGCs through activation of a7 nAChRs. A specific population of cells in the retina, the starburst amacrine cells (SACs), are the only known retinal development, SACs release ACh which is necessary for the production of retinal waves. However, the role of ACh released from SACs in the mature retina is unclear.

If ACh is neuroprotective to RGCs in vitro and SACs are known to release ACh onto the a7 nACH receptors in RGCs of the mammalian retina, do SACs provide endogenous neuroprotection to RGCs? What happens to this transmission of ACh from displaced SACs under glaucoma conditions? Using a well-developed hypertonic glaucoma model in adult rats, this study analyzes changes that occur in the cholinergic synapse between SACs and RGCs in induced glaucoma conditions. It is proposed that the transmission of ACh from SACs onto RGCs provides endogenous neuroprotection to RGCs in the mammalian retina and that this transmission is compromised in glaucoma-like conditions.

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