Abstract
Methamphetamine (MA) is a stimulant to the central nervous system that has highly addictive properties, which can cause an increase in poor health outcomes in those
affected. With a major increase in the use of MA worldwide, these poor health outcomes are becoming more widespread even in New Zealand. In some cases, MA is used by pregnant women, consequently exposing the unborn infant to MA in utero which has been indicated to disrupt growth and development and lead to negative effects later in life. and development and lead to negative effects later in life.There is some research into the specific causes of these effects on growth and development but more needs to be known.
The present study aimed to investigate the effects of in utero MA exposure on brain development. Previous research has indicated a link between MA use and hyperactivity related disorder. Such effects are also associated with changes in the pre-frontal cortex and hippocampus, specifically in changes in neuronal signalling and oligodendrocyte function. The current study looked at Guinea pigs exposed to MA in utero that were then culled and analysed at either Day 0 or Day 28 post birth. These pups were compared to a control group who were not exposed in utero and analysed at the same time points as the exposed pups.
This study highlighted that MA exposure in utero can result in hyperactivity, with a greater response seen in females. Assessment of underlying causes for these behavioural effects were undertaken, with analysis of white matter tracts as evaluated by myelin basic protein staining, which revealed a decrease in staining intensity and volume of white matter tracts that were more predominant in males than females. Assessment of the relationship between parvalbumin positive inhibitory neurons and perineuronal nets on day 0 post birth revealed that females and not males had a much lower level of co-staining than those exposed to MA in utero compared to unexposed controls. However, by 28 days post birth a dramatic increase in the level of co-staining in female exposed to MA was observed compared to controls, whilst males had lower level of costaining in those exposed to MA compared to controls. This study provided evidence that exposure to MA during foetal development hinders brain maturation. This lack of maturation disrupts myelin development, which in turn impedes correct propagation of signalling between brain regions and results in hyperactivity and downstream effects of a lack of neuron stability. These findings are consistent with the current literature on the effects of in utero MA exposure and suggest that there is a specific target for the effects of MA on oligodendrocyte precursor cells that prevents their maturation, which in turn causes a lack of myelination and thus a disruption to signalling through white matter tracts.