Structural and Functional Disorders in Glaucoma: Prospects for Preclinical Diagnosis. Part 2. Electrophysiological Markers of Early Neuroplastic Events

Abstract

Analysis of the literature on the problem of structural and functional relationships in the development and progression of glaucomatous optical neuropathy (GON) shows that the search for a single primary factor may lead to an erroneous exaggeration of its role in the pathogenesis of GON. A more promising approach may be to search for clinically significant combinations of current markers of changes in structure, function, and ocular blood flow, and to expand our fundamental understanding of the processes underlying these changes, designed to improve their interpretation radically. The discussed in this review data of recent studies showed that the earliest event in the development of GON is the weakening and loss of synapses, even with the preserved dendritic branching. We assume that the loss of synapses on dendrites and axon terminals, being a manifestation of synaptic plasticity, may occur simultaneously with the change in anterograde transport in axons of retinal ganglion cells (RGC), or, ahead of it. Early changes in the discharge timing of the RGCs associated with a decrease in the strength of synaptic contacts and the elimination of synapses on dendrites can be a target for neuroprotective therapy. The review analyzes the tests of modern electroretinography, which can serve as markers of early events in the development of GON, including plastic changes in the retina at the preclinical stage of glaucoma, and provides physiological rationales for their selective possibilities for clinical practice.