Correction of morphofunctional retinal damage with dimethylaminoethanol derivatives

Abstract

Glaucoma is a neurodegenerative disease and is the leading cause of blindness worldwide. According to some authors, standard therapy does not always prevent the neurodegenerative process in the retina, which indicates processes that do not depend on intraocular pressure (IOP). The model of NMDA-induced retinal degeneration was chosen by us as one of the main ones for the experimental modeling of glaucoma, due to the fact that glutamate is the main neurotransmitter and triggers excitotoxicity leading to the death of ganglion cells. 7 days after the model the electrophysiological state of the retina was assessed and organs were taken for morphological examination. According to the results of the study, it was found that the compound under the laboratory code DMAE 10-19 had the highest activity. The introduction of the compound led to an improvement in the electrophysiological function of the retina, which consisted in an increase in the amplitude of the wave-a by 34.4 %, the amplitude of the wave-b by 38.2 % relative to the group with the pathology model and has a significant difference (p < 0.05). It also led to an increase in the number of nuclei in the ganglionic layer by 68.8 % relative to the group with the pathology model (p < 0.05). Thus, it was found that the highest neuroprotective activity among dimethylaminoethanol derivatives is observed in the compound under the laboratory code DMAE 10-19. Keywords: dimethylaminoethanol derivatives, NMDA, excitotoxicity, retina, rats, electroretinography, morphometry