A key model for examining the activity-dependent development of primary visual cortex (V1) involves the imbalance in activity between the two eyes induced by monocular deprivation (MD). MD early in life causes dramatic changes in the functional and structural organization of mammalian visual cortex. The molecular signals that mediate the effects of MD on the development of visual cortex are not well defined. Neurotrophic factors are important in regulating the plasticity of visual cortex, but the choice of an appropriate growth factor as well as its delivery has proven difficult. Although vascular endothelial growth factor-B (VEGF-B) is a homolog of the angiogenic factor VEGF-A, it has only minimal angiogenic activity, raising the question of whether this factor has other (more relevant) biological properties. Intrigued by the possibility that VEGF family members affect neuronal cells, we explored whether VEGF-B has a role in the nervous system. In rats, VEGF-B infusion during monocular deprivation (MD) counteracted the normally occurring ocular dominance (OD) shift toward the non-deprived eye so that the deprived eye dominated the VEGF-B-treated cortex after MD. In particular, VEGF-B counteracted the effects of MD without causing detectable alterations in spontaneous discharge or behavior. In conclusion, the simultaneous analysis of visual cortical cell discharge and ocular dominance plasticity suggests that VEGF-B has important effects on the functional architecture of the visual cortex. Therefore, VEGF-B is a new candidate trophic challenge molecule for the visual cortex.Highlights
▸ VEGF-B prevents the shift in ocular dominance distribution in MD rats. ▸ VEGF-B is a potent neurotrophic factor. ▸ VEGF-B treatment did not interfere with the spontaneous activity of V1 neurons.