The key appears to lie with endocannibinoids -- cannabis-like chemicals that are produced by the brain itself, the research showed.
After the prenatal brain is exposed to alcohol, these endocannibinoids impact certain dopamine neurons -- that are involved in addicted behaviours.
The endocannibinoids weaken the excitatory synapses onto dopamine neurons, in the ventral tegmental area (VTA) -- part of the brain implicated in addiction, attention and reward processes.
"The end result is that the dopamine neurons in the brain become more sensitive to a drug of abuse's effect. So, later in life, a person needs much less drug use to become addicted," said Roh-Yu Shen, senior research scientist at the University at Buffalo.
However, in a brain that is prenatally exposed to alcohol, the effect of the endocannabinoids is reduced due to a decreased function of endocannabinoid receptors.
As a result, the excitatory synapses lose the ability to be weakened and continue to strengthen, which Shen believes is a critical brain mechanism for increased addiction risk, Shen said, in the paper detailed in The Journal of Neuroscience.
"By understanding the role endocannibinoids play in increasing the brain's susceptibility to addiction, we can start developing drug therapies or other interventions to combat that effect and, perhaps, other negative consequences of prenatal alcohol exposure," Shen noted.
Prenatal alcohol exposure is the leading preventable cause of birth defects and neurodevelopmental abnormalities.
Foetal Alcohol Spectrum Disorders (FASD) cause cognitive and behavioural problems. In addition to increased vulnerability of alcohol and other substance use disorders, FASD can lead to other mental health issues including attention deficit hyperactivity disorder (ADHD), depression, anxiety and problems with impulse control.