THE ROLE OF TYROSINASE IN THE TIME COURSE OF LIGHT-INDUCED CONE MOVEMENTS IN GOLDFISH RETINA

Abstract

Many teleosts regulate the amount of light incident to the retina through retinomotor movements (RMMs), adjustments of the length of photoreceptors and the distribution of melanin within retinal pigment epithelium (RPE). In the dark, rods contract, cones elongate and pigment aggregates within the basal RPE. In the light, rods elongate, cones contract and pigment disperses within the RPE. It is generally thought that RMMs are regulated by the release of dopamine in the light from tyrosine hydroxylase-containing I1 interplexiform cells (IPCs), acting on D2 family dopamine receptors. However, RMMs are not lost when dopaminergic IPCs are destroyed by injection of the neurotoxin 6-hydroxydopamine (6-OHDA). A potential alternate source of dopamine is the RPE, due to the activity of tyrosinase. In this thesis I tested the hypothesis that light-induced cone contraction depends on tyrosinase activity by treating adult goldfish (Carassius auratus) with the specific tyrosinase inhibitor phenylthiourea (PTU). PTU did not block light-induced cone contraction, nor did 6-OHDA or the combined treatment of PTU and 6-OHDA. However, PTU slowed the progression of light-induced cone contraction as did 6-OHDA, and the slowest extent of progression was achieved when PTU and 6-OHDA were combined. These results suggest that both neuronal (dopaminergic IPCs) and non-neuronal (RPE) dopamine contribute to light-induced cone contraction. That the combined treatment with PTU and 6-OHDA did not block light-induced cone contraction may indicate that one or both of these treatments do not eliminate completely dopamine signalling in the teleost retina, or that light-induced cone contraction may also involve other mechanisms independent of dopamine.