Attention Deficit Hyperactivity Disorder, also known as ADHD, is one of the most common behavioral conditions found in children. Previous research has pointed toward a deficiency in dopamine as the culprit for the symptoms of ADHD. A recent study from the University of Cambridge in the UK used advanced imaging techniques combined with medications that specifically release dopamine to successfully prove that dopamine does not play a role in the expression of ADHD.
In order to understand how dopamine could be involved in ADHD, it’s important to know a little bit more about the molecule. Dopamine is neurotransmitter, so it is synthesized in the brain and released from neurons in response to certain stimuli. Once released, the chemical diffuses toward other nerve cells and activates dopamine-specific receptors on their surfaces. Through this binding, dopamine acts as a chemical courier, relaying signals between multiple neurons. Neural circuits dominated by dopamine release have frequently been implicated in attention, memory, and motivation. These processes overlap smoothly with the deficits found in patients who have ADHD.
To test the role of dopamine in ADHD, researchers first divided participants into two groups: those who have ADHD and those who do not. Within these two groups, half of the subjects were given either methylphenidate – an ADHD drug known more commonly as Ritalin – or a placebo. Ritalin causes an increase of dopamine in the brain, which makes it more available to bind to receptors, thus strengthening the communication between neurons in these circuits.
Participants were instructed to complete tasks that required them to pay attention and concentrate for a period of time before and after taking their dose. The research team found equivalent increases in performance on these tasks across both groups. In addition, using both positron emission tomography (PET) scans and magnetic resonance imaging (MRI) scans, researchers saw equal numbers of dopamine receptors across ADHD and healthy participants, as well as equal amounts of dopamine increase in response to Ritalin across both groups.
This research shows that increases in dopamine, through administration of Ritalin, improves concentration and performance on attention tasks, regardless of the presence of ADHD. Trevor Robbins, a co-author of the study, states: "These findings question the previously accepted view that major abnormalities in dopamine function are the main cause of ADHD in adult patients. While the results show that Ritalin has a 'therapeutic' effect to improve performance, it does not appear to be related to fundamental underlying impairments in the dopamine system in ADHD."
If dopamine is not involved, then what does play a role in ADHD? The imaging techniques used by this research team have added to the body of evidence showing that patients with ADHD have significantly less grey matter when compared to healthy controls. Thus, the problem seems to be of architectural origin, not chemical. The authors of this study hope that their results can facilitate a refocusing on the study of ADHD, and that this will help further the development of ADHD-specific drugs in the future.