Alcohol consumption during pregnancy has negative consequences for the fetus, putting him or her at a higher risk of drug addiction later on in life. In the United States, prenatal alcohol exposure is a leading cause of birth defects and abnormalities associated with neurodevelopment that could easily be prevented.
Fetal Alcohol Spectrum Disorders (FASD) cause behavioral and cognitive problems in children. In addition, FASD can lead to other mental health problems, which include but not limited to anxiety, depression, Attention Deficit Hyperactivity Disorder (ADHD), and impulse control problems. Through a new study, neuroscientists with the Research Institute on Addictions at the University of Buffalo are discovering why prenatal alcohol exposure has this effect on people. Study findings were published in The Journal of Neuroscience.
Prenatal alcohol exposure changes the brain’s reward system. Research shows that this change continues on into adulthood. It appears that the key to the change lies with endocannibinoids, which are chemicals similar to cannabis that the brain produces.
Endocannibinoids play a critical role in the brain’s increasing susceptibility toward addiction. Roh-Yu Shen, PhD and senior research scientist explains that when a brain is exposed to alcohol prenatally, the endocannibinoids affect certain dopamine neurons differently than they would in a prenatal brain that has not been exposed to alcohol. The dopamine neurons are directly involved with addictive behaviors. This causes the brain to become more sensitive to the effects of the abused drug, and then later in life, it will take much less use of a drug to cause the person to become addicted.
In the brain’s ventral tegmental area (VTA), which is an area of the brain associated with attention, addiction, and reward processes, endocannibinoids specifically weaken the excitatory synapses onto dopamine neurons. However, when a brain is exposed to alcohol prenatally, the endocannibinoids effect is reduced because the endocannibinoid receptor function is decreased.
In response to this decreased function of the endocannibinoids, the excitatory synapses can no longer weaken, and instead, continue to strengthen. Shen believes this is a crucial mechanism of the brain that increases a person’s risk of addiction. Shen said that once this chemical change is better understood, drug therapies and other types of interventions could be developed to fight against the effects of prenatal alcohol exposure.
By Trixie Dillwood