Abstract
Abstract: :
Purpose: Glucagon, an amacrine cell neurotransmitter in chicks, inhibits experimental myopia after intraocular administration. Here we tested whether growth–regulation by glucagon requires optic nerve transmission or action in the inner retina. Methods: White Leghorn cockerels (n=6 per group) were kept under a 12:12 hr light/dark cycle. (1) Kainate (KA): Eight days after hatching (P8), treated eyes were injected intravitreally with 200 nmol KA. On P11, 13, and 15, chicks were injected with 20 µL (10–4 M) of (a) glucagon, (b) tetrodotoxin (TTX), (c) glucagon + TTX, or (d) vehicle. (2) Form–deprivation (FD): On P7, treated eyes were covered with a diffuser. On P8, P10 and P12, treated eyes were injected with glucagon and/or TTX as per (1). Control eyes received saline. One day after final treatment, all eyes were refracted, measured, weighed, and fixed for histology and immunocytochemistry. Results: Both KA and FD induced myopia in treated (T) eyes relative to control (C) eyes (T–C= –7.8±0.9 and –11.6±1.3 D, respectively), primarily by enhancing vitreal chamber elongation (T–C= 643±24 and 314±75 µm, respectively). These effects were not altered by TTX. However, glucagon significantly inhibited myopia development, vitreal elongation and equatorial expansion following KA or FD ± TTX. Microscopy showed that KA ablated most amacrine cells and damaged all retinal layers except the pigment epithelium (RPE). TTX caused no detectable damage. Conclusions: Glucagon does not require optic nerve transmission to inhibit KA– or FD–induced myopia, and therefore is unlikely to prevent myopia by acting via inner retinal cells. Glucagon probably acts in the outer retina or RPE to regulate ocular growth.
Keywords: retinal pigment epithelium • retina: proximal (bipolar, amacrine, and ganglion cells) • neuropeptides