Retinal neovascular diseases such as retinopathy of prematurity and proliferative diabetic retinopathy are the major causes of neonatal and adult blindness. During both physiological retinal development and pathological proliferative retinopathy, new blood vessels growth is controlled by VEGF. The inhibitory splice variant VEGF₁₆₅ b is down-regulated in angiogenic tumours (1) and in the vitreous of diabetic patients (R. Perrin, unpublished observations), and is anti-angiogenic in vivo (1). The goal of the present investigation is to examine the role of VEGF₁₆₅ b in retinal neovascularization using a murine model of proliferative retinopathy (2). In this model mice are exposed to hyperoxia, resulting in obliteration of posterior retinal vessels. The mice are then returned to room air, which causes relative hypoxia of the now non-perfused retina, producing a quantifiable neovascular response. For demonstration of fluorescein angiography, C57-BL/6J Mus musculus will be anesthetised with Hypnorm/midazolam (1 part Hypnorm : 2 parts sterile water : 1 part midazolam at the rate 10 ml/kg i.p.) and perfused through the left ventricle with 1 ml of PBS containing 50 mg of 2 x10⁶ *molecular weight FITC dextran. The eyes will be enucleated and fixed in 4% paraformaldehyde. The anterior segment-lens complex will be removed and the posterior eye-cups flat-mounted with the aid of 4 radial full-thickness incisions to yield a Maltese-cross conformation. The flat-mounted retinae will be viewed by epifluorescence microscopy. There will also be a sample demonstration of intravitreal injection of 2μl anti-angiogenic solution under the same conditions of anaesthesia. Treatment of the mice throughout the whole procedure will be conducted in accordance with the ARVO regulations on the Use of Animals in Ophthalmic and Vision Research.