Melatonin protects the optic nerve and the retina against experimental optic neuritis and glaucoma

Abstract

Optic neuritis and glaucoma, prevalent visual dysfunctions with potentially blinding sequels, are the two major degenerative optic neuropathies sharing a common feature, which is retinal ganglion cells loss and axonal damage. Retinal ganglion cells bear the sole responsibility of propagating visual stimuli to the brain. The dysfunction and/or loss of retinal ganglion cells seem to be the primary determinant of irreversible visual loss in optic neuritis and glaucoma. Optic neuritis and glaucoma remain a challenging field to ophthalmologists, as both diseases cause significant morbidity, and the use of traditional ways of treatment is restricted by limited effectiveness and/or considerable side effects. Although optic neuritis and glaucoma differ in several aspects including causes, risk factors, and cell types, among many others, several lines of evidence support that both diseases share some of pathogenic mechanisms such as oxidative damage, excitotoxicity, and inflammation. Melatonin exhibits antioxidant, anti-inflammatory properties, and it has the ability to reduce glutamate synaptic levels. In this chapter, we will discuss evidence supporting the neuroprotective effect of melatonin, a very safe compound (even at high doses) for human use, which prevents and slows the progression of retinal ganglion cell loss, and optic nerve axon damage induced by experimental optic neuritis or glaucoma in rodents, and as such, it could be included in the pharmacological armamentarium of ophthalmic therapeutic resources for the management of these most prevalent forms of optic neuropathy.