A growing number of studies indicate the possible involvement of astrocytes in triggering or modulating neurovascular coupling (NVC), i.e. the local dilation of blood vessels in the brain in response to neuronal activity [1]. Their endfeet, surrounding arterioles and capillaries, are ideally positioned to deliver vasodilators to mural cells, either vascular smooth muscle cells or pericytes. Additionnaly, recent EM data suggest contact between endfeet and synapses [2], indicating direct interactions. At the interface between synapses and vessels, endfeet are perfect candidates to mediate NVC. Recent transcriptomics and proteomics data allowed us to isolate different signaling pathways expressed in astrocytes that can be involved in NVC [3, 4]. Notably, all the enzymes of the Prostaglandin E2 (PGE2) pathway were expressed. Despite the data available in the literature, NVC remains poorly understood. Computational modeling works have contributed to improving our understanding of the role of astrocytes in NVC, showing for example that potassium signaling can trigger a rapid response whereas nitric oxide is slower [5]. To the best of our knowledge, there is no astrocyte model implementing the entire arachidonic acid (AA) release, from membrane lipids to PGE2. Based on previous models [5, 6], we implement a new model of astrocyte-mediated NVC that includes the PGE2 pathway. We show that this pathway could be responsible for the ’late’ but not the ’early’ response of NVC at the arteriolar level recently observed experimentally [7]. This work supports the hypothesis that the PGE2 pathway in astrocytes can trigger the late response of NVC to prolonged stimulation. A spatialization of the model will be performed to investigate the role of local NVC signaling at the endfoot level in effectively maintaining hyperemia.