Since 1999, there has been a dramatic increase in opioid overdose deaths and addiction to opioid drugs, including both prescription opioid pain relievers and heroin. Increased rates of addiction have also been seen among pregnant women, which has led to a significant increase in the number of babies born with neonatal abstinence syndrome. Methadone is a long-acting opioid that is an effective treatment for addiction to opioid drugs and is often used to treat pregnant women. While methadone treatment is safer than non-medical use or abuse of opioids, it is known that methadone can cross the placenta, and little is known about the effects of methadone on an infant’s developing brain.
During development, some brain cells, including oligodendrocytes, express opioid receptors that bind opioid drugs such as methadone. Oligodendrocytes are involved in multiple complex functions critical to normal brain development, including production of myelin, a substance that enables neurons to send electrical signals and communicate with other cells. In this study, researchers examined the effects of methadone on oligodendrocytes during development in an animal model. Rat pups were exposed to methadone both through the placenta and through maternal milk until postnatal day 14, a period that is equivalent to the third trimester in human pregnancy. The researchers found that therapeutic doses of methadone caused increases in multiple proteins found in myelin and an increase in number of neurons with mature myelin. This accelerated maturation and myelination could potentially disrupt normal connectivity within the developing brain.
These results highlight the importance of understanding how drugs that are used to treat addiction might impact the developing brain of infants prenatally exposed to them. They also raise questions about the impact of methadone on the adolescent brain, which is also still developing.
Study:
The Opioid System and Brain Development: Effects of Methadone on the Oligodendrocyte Lineage and the Early Stages of Myelination, Dev Neurosci 2014;36:409–421 http://www.ncbi.nlm.nih.gov/pubmed/25138998