Changes of electroretinogram response in myopia model of guinea pigs treated with different concentrations of atropine

Abstract

With the popularization of electronic products and protracted near-work time, the prevalence of myopia is increasing all over the world, especially among young children. The incidence of myopia and development of means of controlling it represent a research hotspot in the field of ophthalmology. Research up to the present shows the most effective means of mitigating myopia progression: anti-muscarinic topical medications, but the exact mechanism is unknown. Atropine, a kind of nonspecific muscarinic antagonist, can significantly hamper myopia progression. The present investigations have demonstrated that the possible mechanism of atropine is the action on certain nerve cells on the retina and affects the transmission of their neurotransmitters. Electrophysiological examination of the retina can indicate the function and state of the retinal cells. Through using the knowledge of the origin of various components of the electroretinogram, we are able to assess the effects of medication on different retinal cells and layers. In this investigation, we aimed to understand the pharmacological mechanisms of retarding myopia progression by administrating different concentrations of atropine eyedrops to lens-induced myopic guinea pig eyes via electrophysiological techniques. 36 postnatal 14-day-old guinea pigs were randomly assigned to 3 groups: 1% Atropine group, 0.01% Atropine group and the vehicle group, with 12 animals in each group. The myopia model of guinea pigs was established using -10.00D spectacle lenses to cover the right eye. From the beginning of week 2, the right eye of each animals with - 10D spectacle lenses received the eyedrop treatment: 1 drop of atropine 1%, 0.01% or vehicle eye drops, respectively in each experimental group, once in the morning until week 8. All animals in each group underwent refraction and ERG measurement at each of week 2, 4, 6 and 8. Myopic shift was established in the right eye throughout the entire experimental period, whereas emmetropization was achieved in the left eye at approximately week 4. The myopic level was decreased in the atropine-treated eyes in a dose-dependent manner. The ERG results showed that photopic b-wave amplitude and the b/a wave ratio was increased by atropine treatment in a dose-dependent manner during week 6 and 8. Based on the following facts: (1) Since atropine eyedrops were administrated, the photopic b-wave amplitude and b/a ratio increased in 0.01% and 1% atropine eyedrops; (2) In vehicle group, Paired analysis of the left and right eyes showed that the statistical significances of photopic b wave amplitude and b/a ratio weren’t detected at all experimental timepoints. However, in 0.01% atropine and 1% atropine group statistical significance appeared at week 6 and 8. (3) The photopic b-wave amplitude was statistically significant but the scotopic b-wave amplitude was not. Therefore, we draw the conclusion that the main site of action of atropine eyedrops for controlling myopia development is in the cells that produce the photopic ERG b-wave. This finding suggests a mechanism of action of atropine on myopia and indicates alternative strategies for developing more effective interventions to prevent and control myopia in the future. (494 words)