NEW YORK, Nov 16 (Reuters Health) -- Attention-deficit/hyperactivity
disorder may be the result of damage to part of an unborn child's brain
that is caused by a mother's alcohol intake during pregnancy. The part of
the brain damaged before birth involves a complex communication system
between nerve cells, investigators suggest in the November issue of
Alcoholism: Clinical & Experimental Research.
Led by Dr. Roh-Yu Shen of the State University of New York at
Buffalo, researchers examined the apparent consequences of exposure before
birth to alcohol in experimental rats.
"We have found that the electrical activity of... dopamine neurons
(in the brain) is reduced in the offspring (of pregnant rats treated with
alcohol)," Shen told Reuters Health in an interview. "These neurons
normally generate a certain amount of spontaneous electrical activity...
(resulting) in dopamine (release) in brain areas... responsible for
attention."
Dopamine is one of a number of natural chemical substances called
neurotransmitters that help transmit impulses across the synapse, or gap,
between nerve cell endings.
"We think that attention/hyperactivity problems... may be caused by
the reduced activity in (these) dopamine neurons," Shen explained. She and
her colleagues have observed no structural differences in the areas where
these neurons are situated, no loss or destruction of neurons, but rather
"reduced activity" of the cells in both young and adult animals.
Though the precise sequence of events that leads to
attention-deficit/hyperactivity disorder (ADHD) is unknown, Shen believes
that "alcohol exposure impairs the development of brain dopamine neurons."
This impairment ultimately results in a decrease in the quantity of
dopamine released in areas of the brain that control attention and the
ability to focus.
According to Shen, the new study results strongly suggest that
"substances of abuse could lead to mental deficits... such as ADHD... in
the offspring," deficits that continue beyond childhood. In her view,
"clinicians might want to reexamine the notion that ADHD may be 'outgrown'
(since) a reduced dopamine function is a persistent phenomenon during
adulthood. It may simply take a more subtle form," she added.
Shen explained that the "rat model provides us (with) a systematic
approach to investigate the therapeutic potential of (various)
pharmacologic agents in ADHD following fetal alcohol exposure." She cited
Ritalin as an example of a stimulant drug whose properties may be useful in
treating alcohol-induced ADHD.
She commented further that this experimental model would be employed
in her team's ongoing research efforts to "study how stimulants can
'restore' the deficits in dopamine neuron activity."
Shen noted that substances such as cocaine and certain psychiatric
medications also reduce dopamine neuron activity, and "any events that
disrupt dopamine neurons during fetal development, for example, stress,
(could) lead to dysfunction of (these) neurons and ADHD."
