Rewards are a necessary part of human life; they are critical for behaviour and everyday functioning. Importantly, reward processes are also associated with the release of the feel good hormone – dopamine. For example, a simple task such as getting up for work in the morning, although may be momentarily undesirable is influenced by the prospect of a reward – which of course is the pay check at the end of the month. The ability therefore to think ahead, visualize and keep in mind the monetary reward – despite the fact that it is a future, delayed reward as opposed to an immediate one – provides most people with sufficient motivation to get out of bed each morning and go to work. In fact, rewards play a prominent feature in many other aspects of our lives. For example, we are rewarded when enjoying a delicious meal via the release of dopamine and therefore motivation for food is inherent. Exercise is also rewarding and releases a fusion of feel good hormones. More on the role of exercise in ADHD is discussed in the ADHD and associated behaviors section of the website.
In the previous section, we learnt that the ventral striatum is considered the reward center of the brain, although other brain regions including the nucleus accumbens and ventro-striatal nucleus are also implicated. Neuroimaging studies using tasks measuring reward-related responses have shown observable differences in children and adults with ADHD compared to controls. The differences in brain function are referred to as – hypo-activation, that is reductions in task-specific activation of the ventral striatum during tasks of reward processing and suggest some impairment in this function [18-20]. There are an abundance of dopamine derived D2 receptors in the stiatum which are thought to play a critical role in reward processes .
A recent survey by an initiative carried out by Closing the Addiction Treatment Gap (CATG) estimated that 23, million Americans over the age of 12 have an addiction to alcohol or other drugs. One in four adults in England are thought to drink alcohol to harmful levels, and one in 20 are “dependent drinkers”, according to the Think Tank: the Centre for Social Justice (CSJ). While, estimates of drug use were reported by DrugScope in 2009 to be around 1.2 million people over the age of 18. In relation to their mechanism of action, addictions such as those to nicotine, alcohol and cocaine are directly related to dopamine release. In fact, nicotine acts mechanistically remarkably like cocaine in the brain. In short, cocaine works by blocking dopamine transporter sites in the terminal buttons of neurons and in doing so prevents the reuptake of dopamine by the neurons that release it. This enables higher concentrations of dopamine to remain in the synapse for an extended period of time resulting in a high/feelings of euphoria.
Reward pathways. The mesolimbic and mescoritical tracts are considered the reward pathways of the brain. They are formed by dopaminergic neurons which project to the amygdala and hippocampus  and are involved in the regulation of emotion and motivation related processes. There is some current evidence suggesting that (i) impulsive behaviours; (ii) addictions to drugs of abuse and (iii) symptoms of ADHD are independently associated with impairments in striatal dopamine signalling, e.g., poor D2 receptor binding and dopamine release .
Interestingly, inadequate or deficient levels of the omega-3, DHA, results in a significant decrease in the density of ventral striatal D2 -like receptors . This raises questions concerning the role of omega-3 and perhaps, DHA specifically in dopamine activity. However, to date, the relationship between omega-3 and dopamine is not well elucidated. Furthermore, it remains unknown whether dietary supplementation in humans with high doses of omega-3 HUFAs can restore the ventral striatal D2 receptor signalling pathways and in doing so mediate addictive, motivational and reward-related behaviours.