Dopamine (DA), which is a catecholamine neurotransmitter released by DA neurons, is associated with addiction and is responsible for many biological functions including cognition, learning, motor control, motivation, and reward. Although previous studies were helpful to understand the general mechanism of the reward system within the midbrain area, the underlying mechanisms at the molecular and cellular levels during early maturation in response to perinatal substance abuse were not investigated and integrated. Thus, there remains an unmet need to develop novel technologies to better understand the molecular and cellular mechanism underlying the midbrain reward pathway in response to perinatal substance abuse during early maturation.
Our preliminary data suggests that dopamine neurons, in response to nicotine exposure during pregnancy, were significantly activated, allowing the release of unusually high levels of dopamine in the prefrontal cortex. Active dopamine, known as the feel-good hormone, is a neurotransmitter that carries information between neurons and regulates emotional responses, particularly those related to rewards, which could play a part in addiction. We hypothesize that the impacted (altered) dopamine pathways could result in babies being born addicted to nicotine.
To monitor the neural activation within the sub-regions of the VTA, we recentlyproposed and developed a novel microimaging device that can be directly implanted into the brain. We believe that our approach will help us to better understand the effect of maternal nicotine and alcohol exposure on DA neurons within the sub-regions of the VTA at both cellular and molecular levels during early maturation. Subsequently, this could expand our understanding of the reward pathway and can lead to the development of novel drugs to assist with substance abuse cessation.