Oligodendrocytes are the myelinating cells of the central nervous system. The long-lasting view of their function is to increase the velocity of action potential propagation. Recently it was postulated that oligodendrocytes could also support the underlying axon metabolically. A current model shows that electrically active axons activate oligodendroglial NMDA receptors. This leads to increased calcium levels in oligodendrocytes and to translocation of glucose transporters to the oligodendroglial plasma membrane. NMDAR-induced glucose transported translocation results in increased glucose uptake and increased lactate production for axonal metabolic support. Since oligodendrocytes sense the activity of electrical active axons, and because those axons are isolated from the extracellular milieu and from astrocytes, we hypothesize that oligodendrocytes participate in neurovascular coupling in the white matter by relaying axonal activity to the vasculature. Following the previous model, we would like to test the necessity of oligodendroglial NMDA receptors for functional hyperemia in the white matter, and to identify the cellular mechanisms of neurovascular coupling in the white matter. To answer these questions, I establish an ex vivo system for neurovascular coupling studies using the murine optic nerve. By labelling the vessels with Dextran-TexasRed and IB4-Lectin, I can observe the localization of pericytes and thus target my imaging area to different parts of the vascular tree. By using three different electrophysiological frequencies, I observed dilation on control animals, which is absent in NMDA receptor knock out animals. By using acetylcholine, as positive control for vessel dilation, I observed dilation in both genotypes, indicating that oligodendroglial NMDA receptor plays a crucial role in neurovascular coupling in white matter. The preliminary results indicate that oligodendroglial NMDAR are essential for white matter functional hyperemia, a phenomenon that is vastly understudied.