Νeuronal and glial cells play an important role in the development of vasculature in the retina. In this study, we investigated whether re-vascularization occurs in
retinal neurodegenerative injury models. To induce
retinal injury,
N-methyl-D-aspartic acid (
NMDA, 200 nmol) or
kainic acid (KA, 20 nmol) was injected into the vitreous chamber of the eye on postnatal day (P)7. Morphological changes in retinal neurons and vasculature were assessed on P14, P21, and P35. Prevention of vascular growth and regression of some capillaries were observed on P14 in retinas of
NMDA- and KA-treated eyes. However, vascular growth and re-vascularization started on P21, and the
retinal vascular network was established by P35 in retinas with neurodegenerative
injuries. The re-vascularization was suppressed by a two-day treatment with
KRN633, an inhibitor of
VEGF receptor tyrosine kinase, on P21 and P22. Astrocytes and Müller cells expressed
vascular endothelial growth factor (
VEGF), and the distribution pattern of
VEGF was almost the same between the control and the
NMDA-induced
retinal neurodegenerative injury model, except for the difference in the thickness of the inner
retinal layer. During re-vascularization, angiogenic sprouts from pre-existing blood vessels were present along the network of
fibronectins formed by astrocytes. These results suggest that glial cells contribute to angiogenesis in neonatal rat models of
retinal neurodegeneration.