The balance between the quiescent and activated states of adult neural stem/progenitor cells (NSPCs) is crucial for maintaining sustained neurogenesis throughout life. NSPCs mostly remain quiescent during adulthood but can proliferate in response to specific stimuli. While cellular metabolism has emerged as a key factor in determining the activity state of stem cells, its precise role in orchestrating the transition from quiescence to proliferation in NSPCs is not fully understood. Generally, stem cells rely on glycolytic metabolism to support the synthesis of cellular building blocks necessary for cell growth. However, during differentiation, there is a shift towards oxidative metabolism, which also appears to be important for adult NSPCs. Our study uncovers a crucial and unexpected role played by the mitochondrial pyruvate carrier (MPC) in the regulation of this process. MPC transports the key metabolite pyruvate into mitochondria, establishing a link between cytosolic glycolysis and mitochondrial oxidative metabolism. We show that quiescent NSPCs possess active mitochondrial metabolism and express high levels of MPC. The entry of pyruvate into the mitochondria is necessary to maintain NSPCs in a quiescent state. Indeed, the inhibition of pyruvate transport into mitochondria triggers their activation and increases intracellular levels of aspartate, despite a significant decrease in TCA cycle intermediates. Furthermore, NSPCs lacking MPC have the ability to differentiate into mature neurons, indicating a remarkable metabolic flexibility that allows these cells to adapt their metabolism based on substrate availability. In conclusion, we have shown that deleting MPC in NSPCs enhances neurogenesis in adult and aged mice.