A study using mice provides insight into how a specific receptor subtype in the brain could play a role in increasing a person's risk for attention-deficit hyperactivity disorder (ADHD). The research, conducted by the Intramural Research Program (IRP) at the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, could also help explain how stimulants work to treat symptoms of ADHD.
Dysfunction of the dopamine D4 receptor subtype is linked to ADHD as well as other disorders characterized by decreased impulse control, including drug abuse. One subtype variant, D4.7, has been of particular interest because of its increased prevalence in those diagnosed with ADHD. However, the function of this particular variant in ADHD has been poorly understood.
In the study, published in today's Molecular Psychiatry, researchers inserted three variants of the dopamine D4 receptor into cells and into mice so that they could investigate differences in biological activities. The researchers found that the D4.7 variant, unlike its D4.2 and D4.4 counterparts, was not able to interact with the short version of the dopamine type 2 (D2S) receptor to reduce glutamate release in a brain region associated with impulsivity and symptoms of ADHD in humans.
"Although previous studies have shown that dysfunctional dopamine D4 receptors are implicated in ADHD, this is the first study to show how this genetic difference might translate into functional deficits seen with this disorder," said NIDA Director Dr. Nora D. Volkow. "Further research is needed to explore how this deficient interaction between receptors might be remedied, which could then lead to new medications for the treatment of ADHD."
Children with ADHD have trouble paying attention and controlling impulsive behaviors, and may be overly active, often resulting in poor school performance and social difficulties. They are also at increased risk for substance use disord
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NIH/National Institute on Drug Abuse