In the brain's grey matter, astrocytes have been suggested to export lactate to neurons to power their mitochondria. In the white matter, lactate can support axon function in conditions of energy deprivation, but it is not known whether lactate works by preserving energy levels in axons or in oligodendrocytes, the myelinating processes of which are damaged rapidly in low energy conditions. Studies of cultured cells suggest that oligodendrocytes are the cell type in the brain which consumes lactate at the highest rate, in part to produce membrane lipids presumably for myelin. Here we use pH imaging to show that oligodendrocytes in the white matter of the cerebellum and corpus callosum take up lactate via monocarboxylate transporters (MCTs), which we identify as MCT1 by immunocytochemistry and electron microscopy. Using cultured slices of developing cerebral cortex from mice in which oligodendrocyte lineage cells express GFP under control of the Sox10 promoter, we show that a low glucose concentration inhibits myelination. This inhibition is enhanced when lactate uptake is blocked with D-lactate, and is reduced when exogenous L-lactate is supplied. These data suggest that oligodendrocytes can take up lactate using MCT1 and use it to support myelination. In CNS diseases involving energy deprivation at times of myelination or remyelination, as occurs in conditions causing periventricular leukomalacia leading to cerebral palsy, in stroke, and in secondary ischaemia following spinal cord injury, lactate transporters in oligodendrocytes may play an important role in minimising the inhibition of myelination that occurs.