Retinal neovascularisation is a major clinical complication of diabetic retinopathy (DR) however, the exact mechanism for the progression of retinal neovascularisation and the role of inflammation in retinal neovascularisation remains to be established. There are two main hypotheses on the pathogenic mechanism underlying DR. The more established theory which has been the focus of many studies is that DR is a disorder affecting the vascular cells in the retina. It is theorised that damage to these cells as a consequence of hyperglycaemia result in the subsequent complications of DR including vision loss. The other theory is that DR causes neuronal and glial cell dysfunction which plays a crucial role in the progression of the subsequent complications. Evidence suggesting neuronal and glial cell dysfunction include; changes in electrophysiological and psychophysical activity, glial cell reactivity, altered glutamate metabolism and apoptosis of retinal cells. The aim of this project is to investigate the neuronal and glial cell changes in the retina in a transgenic mouse model of retinal neovascularisation and to assess the relationship between the vascular abnormalities with the corresponding changes in the neurons and glial cells. The transgenic mouse model, Kimba (Lai et al 2005), was used to examine the neuronal and glial cell changes in retinal neovascularisation. Retinal sections of Kimba and wild type (WT) mice were analysed for vascular neuronal and glial cells changes using immunocytochemistry. Mice aged 2, 8, and 20 weeks were used to look at neuronal and glial changes associated with the progressive stages of neovascularisation.There was an overall decrease in retinal thickness for Kimba mice at all stages with varying patterns of changing thickness in the outer nuclear layer (ONL) and inner nuclear layer (INL) of the retina. Compared to WT, the retinal blood vessels in Kimba mice transgressed into the outer layers of the retina including the ONL which caused disruption to the normally organised retinal layers. There was a significant (P<0.001) decrease in ganglion cell count in Kimba at all age points. Whilst there was no change in the morphology of astrocytes and Muller cells, there was a significant (P<0.05) decrease in Müller cell count in 8 and 20 weeks Kimba. The study shows changes in both neuronal and glial cells in the retina associated with the different stages of retinal neovascularisation. This study further supports the role of inflammation in the progression of retinal neovascularisation.