Atropine restores retinal glutamate / γ-aminobutyric acid levels in vitro in an experimental chick model of myopia.

Abstract

Atropine is widely used to slow childhood myopia progression, but its mechanisms of action remain poorly understood. This study investigated atropine's effects on retinal neurochemistry in a chick model of form-deprivation myopia (FDM). Myopia was induced in chicks via monocular FDM. Retinas from FDM and contralateral normal eyes were enucleated, bisected and six retinal samples per group were incubated for 60 min in vitro in either 1.8 mM atropine or normal physiological buffer. Samples were fixed in glutaraldehyde for neurotransmitter detection using silver-intensified immunogold labelling. In a separate experiment, the incubation procedure of FDM and normal eyes was repeated and tissues were fixed in formaldehyde to examine dopaminergic neurons using tyrosine hydroxylase (TH) immunofluorescence. No significant changes in TH immunolabelling were observed between groups. However, myopia reduced glutamate levels by 43% compared to controls, with altered glutamate distribution in the inner retina. Bipolar cells in myopic eyes also showed a 57% decrease in glutamine levels. Within 60 min, atropine treatment restored both glutamate and glutamine levels toward normal levels. The most noteworthy changes to gamma aminobutyric acid (GABA) was a 62% reduction observed in the outer plexiform layer (OPL) between normal and myopic retinas. Following atropine treatment, there was a further decrease in (GABA) levels in OPL and horizontal cells. These findings suggest that one immediate effect of atropine treatment is to restore the balance of neurotransmitters that are disrupted in myopia, elevating glutamate while reducing GABA. This neurotransmitter modulation may contribute to atropine's therapeutic effects in myopia control.