Neural activity-regulated myelin plasticity is increasingly recognized as a dynamic regulator of neural circuit function shaping cognition and learning. However, its role in pathological circuit remodelling remains largely unexplored. Drugs of abuse, including opioids such as morphine, target the dopaminergic reward system and drive persistent synaptic and circuit-level modifications. Although microglia and astrocytes have been implicated in these adaptations, the contribution of myelin-forming oligodendroglial lineage cells, which are uniquely positioned to modify circuit function, has remained unknown. In this talk, I will discuss our findings demonstrating that myelin plasticity is a key modulator of dopaminergic circuit function and opioid reward. Increased dopaminergic neuron activity, evoked by either optogenetic stimulation or morphine, induces oligodendrogenesis within the reward system in a circuit- and region-specific manner. Disrupting this myelin plasticity through conditional blockade of oligodendrogenesis abrogates morphine-associated reward learning, identifying oligodendroglial cells as critical regulators of reward behaviour. Real-time dopamine recordings reveal that myelin plasticity is necessary for modulating network synchrony and ensuring a timely dopamine release required for reward learning. Our findings establish myelin plasticity as a previously unappreciated feature of dopaminergic reward circuitry that critically contributes to the behavioural reinforcing effects of opioids.