Administration of opioids such as morphine induces long-lasting maladaptive changes to neurotransmission in the brain’s reward circuitry — specifically, the ventral tegmental area (VTA) → nucleus accumbens (NAc) reward pathway — leading to the development of opioid-use disorders. The roles of oligodendroglial lineage cells and myelination status in these maladaptive circuit changes, and their consequent effects on conduction velocity and circuit properties, are not well understood.

In this study, Yalçın et al. looked at activity-dependent changes in myelination of the VTA → NAc pathway in mice using three approaches that increased activity of this pathway: morphine-induced conditioned place preference (CPP; a behavioural paradigm for studying reward-based learning), optogenetic activation of VTA dopaminergic neurons, and disinhibition of GABAergic neurons in the VTA. All three approaches resulted in oligodendrogenesis in the VTA (but not along the distal portions of the projecting axons or downstream in the NAc), demonstrated by increases in oligodendrocyte precursor cell (OPC) proliferation, oligodendrocyte numbers and myelination.