Abstract
Acetylcholine (ACh) release by starburst amacrine cells (SACs) has been implicated in the production of retinal waves during early retinal development. Inhibitory gamma-aminobutyric acid (GABA) release by SACs is known to be involved in directional selectivity in the mature retina. However, the role of SAC release of acetylcholine in the adult developed mammalian retina is not entirely understood. Some evidence suggests a neuroprotective effect on retinal ganglion cells (RGCs) acting through alpha7 nicotinic acetylcholine receptors (nAChRs) present in RGCs. If ACh released by SACs is neuroprotective to RGCs, it would follow that this cholinergic transmission might be compromised in glaucoma conditions, at a time point prior to RGC loss. In this study, hypertonic saline injections into the episcleral veins surrounding the eyes of adult Long Evans rats were made to induce glaucoma-like conditions.
Highlights
Glaucoma is a group of degenerative retinal diseases characterized by progressive loss of retinal ganglion cells (RGCs) and their axons that make up the optic nerve leading to irreversible loss of vision
The results from this study provide evidence of apoptotic loss of displaced starburst amacrine cells (SACs), corresponding with a reduction in ACh content and α7 nicotinic acetylcholine receptors (nAChRs) before any significant loss of RGCs occurs in an in vivo rat glaucoma model
Is the loss of SACs and reduction of ACh a factor in the eventual loss of RGCs associated with glaucoma? If so, these results provide insight into the identification of a possible new function for cholinergic amacrine cells within the adult mammalian retina
Summary
Glaucoma is a group of degenerative retinal diseases characterized by progressive loss of retinal ganglion cells (RGCs) and their axons that make up the optic nerve leading to irreversible loss of vision. As a leading cause of irreversible blindness in the world, it is estimated that there will be 79.6 million patients with glaucoma by 2020 [1]. The primary risk factor of glaucoma is an increase of intraocular pressure (IOP) and all current treatments are designed to lower IOP [2,3,4]. These treatments alone are often unable to stop the progression of vision loss asso-.
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