One of the many negative consequences when fetuses
are exposed to alcohol in the womb is an increased
risk for drug addiction later in life.
Neuroscientists in the University at Buffalo
Research Institute on Addictions are discovering
New research suggests the reason fetal exposure to
alcohol increases the risk of drug addiction later
in life may be related to endocannibinoids,
cannabis-like chemicals that the brain itself
Through a research grant from the National Institute
on Alcohol Abuse and Alcoholism (NIAAA) of the
National Institutes of Health (NIH), Senior Research
Scientist Roh-Yu Shen, PhD, is studying how prenatal
alcohol exposure alters the reward system in the
brain and how this change continues through
“By understanding the role endocannabinoids 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 says.
Fetal Alcohol Spectrum Disorders (FASD) cause
cognitive and behavioral 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.
“After the prenatal brain is exposed to alcohol, the
endocannabinoids have a different effect on certain
dopamine neurons which are involved in addicted
behaviors than when brain is not exposed to
alcohol,” Shen says.
“The end result is that the dopamine neurons in the
brain become more sensitive to a drug of abuse’s
So, later in life, a person needs much less drug use
to become addicted.”
Specifically, in the ventral tegmental area (VTA) of
the brain, endocannabinoids play a significant role
in weakening the excitatory synapses onto dopamine
The VTA is the part of the brain implicated in
addiction, attention and reward processes.
However, in a brain 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’s research appears in the latest issue of The
Journal of Neuroscience.
Kathryn Hausknecht, RIA research assistant, was the
lead author of the article, with Ying-Ling Shen,
PhD, former postdoctoral fellow, Rui-Xiang Wang, PhD
candidate, UB Department of Psychology, Samir
Haj-Dahmane, PhD, RIA senior research scientist and
co-investigator, and Shen as co-authors.
For more information
The Journal of Neuroscience
Prenatal Ethanol Exposure Persistently Alters
Endocannabinoid Signaling and Endocannabinoid-Mediated
Excitatory Synaptic Plasticity in Ventral Tegmental
Area Dopamine Neurons
University at Buffalo