Literature DB >> 27523467

Evaluating retinal ganglion cell loss and dysfunction.

Ben Mead1, Stanislav Tomarev2.   

Abstract

Retinal ganglion cells (RGC) bear the sole responsibility of propagating visual stimuli to the brain. Their axons, which make up the optic nerve, project from the retina to the brain through the lamina cribrosa and in rodents, decussate almost entirely at the optic chiasm before synapsing at the superior colliculus. For many traumatic and degenerative ocular conditions, the dysfunction and/or loss of RGC is the primary determinant of visual loss and are the measurable endpoints in current research into experimental therapies. To actually measure these endpoints in rodent models, techniques must ascertain both the quantity of surviving RGC and their functional capacity. Quantification techniques include phenotypic markers of RGC, retrogradely transported fluorophores and morphological measurements of retinal thickness whereas functional assessments include electroretinography (flash and pattern) and visual evoked potential. The importance of the accuracy and reliability of these techniques cannot be understated, nor can the relationship between RGC death and dysfunction. The existence of up to 30 types of RGC complicates the measuring process, particularly as these may respond differently to disease and treatment. Since the above techniques may selectively identify and ignore particular subpopulations, their appropriateness as measures of RGC survival and function may be further limited. This review discusses the above techniques in the context of their subtype specificity.
Copyright © 2016 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Dysfunction; Electroretinography; Quantification; Retina; Retinal ganglion cells; Visual evoked potential

Mesh:

Year:  2016        PMID: 27523467      PMCID: PMC5045805          DOI: 10.1016/j.exer.2016.08.006

Source DB:  PubMed          Journal:  Exp Eye Res        ISSN: 0014-4835            Impact factor:   3.467


  113 in total

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5.  Activation of 5-HT1A Receptors Promotes Retinal Ganglion Cell Function by Inhibiting the cAMP-PKA Pathway to Modulate Presynaptic GABA Release in Chronic Glaucoma.

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9.  Axonopathy precedes cell death in ocular damage mediated by blast exposure.

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