Abstract
Purpose: :
In previous studies in chicks, monocular atropine was found to inhibit lens-induced myopia (LIM) in both treated and fellow untreated eyes. To investigate the role of central regulatory pathways in this "yoked" response, we studied the effect on the latter of sectioning the optic nerve, to prevent communication between the retina of the lesioned eye and the brain.
Methods: :
Unilateral optic nerve section (ONS) and sham surgeries were performed on 11-day-old White-Leghorn chicks. Six days later, -10D lenses were fitted to ONS and sham eyes. Monocular 10µl intravitreal injections of either atropine (750µg) or vehicle (dH2O) were performed daily for a period of 4 successive days, on either the lens- (ipsilateral, IL) or non-lens (contralateral, CL) wearing eyes. Refractive errors (RE) were measured using retinoscopy and axial dimensions, with high frequency A-scan ultrasonography. All procedures were performed under isoflurane (1.5% in oxygen) anesthesia.
Results: :
Eye growth, shown as differences between endpoint and baseline data, (mean±SD), was significantly inhibited by IL and CL atropine. With sham surgery, changes in refraction (RE) and axial length (AL) with vehicle (control) were -8.01±3.96D and 0.808±0.243mm, and with atropine, were -1.53±3.03D and 0.56±0.35mm (IL), and -2.65±2.13D and 0.52±0.16mm (CL). The atropine groups were not significantly different from each other (p=0.23, RE; 0.42, AL) but were different from the vehicle group (p=0.0003, RE; 0.016, AL). The inhibitory effect of CL atropine was abolished by ONS on the lens-wearing eye; these ONS eyes were similar to sham controls (-8.58±2.07D, p=0.56, RE; 0.88±0.12mm, p=0.18, AL).
Conclusions: :
Our results indicate that an intact optic nerve is essential for the contralateral inhibitory effect of atropine on LIM, opening the possibility that a central neuronal pathway mediates this yoked response.
Keywords: myopia • optic nerve • second messengers: pharmacology/physiology