Research has shown that prenatal exposure to alcohol can lead to an increased risk for drug addiction later in life. Now neuroscientists at the University at Buffalo Research Institute on Addictions are discovering the underlying mechanisms for why this occurs.
Specifically, the researchers are investigating how prenatal alcohol exposure changes the reward system in the brain and how this alteration impacts a person throughout adulthood. The key appears to lie with endocannibinoids, cannabis-like chemicals that are produced by the brain itself.
The researchers found that once the fetus’s brain is exposed to alcohol, the endocannibinoids will exert a different effect on the dopamine neurons associated with addictive behaviors. These dopamine neurons become more sensitive to the effects of the drug, so this person would need much less of the drug to become addicted.
“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,” said Senior Research Scientist Roh-Yu Shen, Ph.D.
Prenatal alcohol exposure is the leading preventable cause of birth defects and neurodevelopmental abnormalities in the United States. Babies born with fetal alcohol spectrum disorders (FASD) can have a range of developmental, cognitive and behavioral disorders. Some exhibit physical abnormalities upon birth, such as a smaller head size and irregular facial features.
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.
Specifically, endocannibinoids play a significant role in the ventral tegmental area (VTA, a part of the brain associated with addiction, attention and reward processes, in that they weaken the excitatory synapses on the dopamine neurons.
But in a brain prenatally exposed to alcohol, the impact 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 an important reason for increased addiction risk.
“After the prenatal brain is exposed to alcohol, the endocannibinoids have a different effect on certain dopamine neurons which are involved in addicted behaviors than when brain is not exposed to alcohol,” said Shen.
“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.”
Source: University at Buffalo
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