associated with difficulties preparing to act, switching between response alternatives, and inhibiting inappropriate responses. Recent research has uncovered additional regions of interest, as well as highlighted particular subregions of the PFC, that can be tied to performance in specific behavioral tasks. Delay discounting Excitotoxic lesions in the nucleus accumbens core have been shown to increase preference for the smaller, immediate reward, whereas lesions to the nucleus accumbens shell have had no observable effect. Additionally, lesions of the basolateral amygdala, a region tied closely to the PFC, negatively affect impulsive choice similarly to what is observed in the nucleus accumbens core lesions. Moreover, dorsal striatum may also be involved in impulsive choice in an intricate manner. Go/No-go and Stop-signal reaction time test The orbitofrontal cortex is now thought to play a role in disinhibiting, and injury to other brain structures, such as to the right inferior frontal gyrus, a specific subregion of the PFC, has been associated with deficits in stop-signal inhibition. 5-Choice Serial Reaction Time Task (5-CSRTT) and Differential Reinforcement of Low rates (DRL) As with delay discounting, lesion studies have implicated the core region of the nucleus accumbens in response inhibition for both DRL and 5-CSRTT. Premature responses in the 5-CSRTT may also be modulated by other systems within the ventral striatum. In the 5-CSRTT, lesions of the anterior cingulate cortex have been shown to increase impulsive responding, and lesions to the prelimbic cortex impair attentional performance. Iowa Gambling Task Patients with damage to the ventromedial frontal cortex exhibit poor decision-making and persist in making risky choices in the Iowa Gambling Task. Neurochemical and pharmacological findings The primary pharmacological treatments for ADHD are methylphenidate (Ritalin) and amphetamine. Both methylphenidate and amphetamines block re-uptake of dopamine and norepinephrine into the pre-synaptic neuron, acting to increase post-synaptic levels of dopamine and norepinephrine. Of these two monoamines, increased availability of dopamine is considered the primary cause for the ameliorative effects of ADHD medications, whereas increased levels of norepinephrine may be efficacious only to the extent that it has downstream, indirect effects on dopamine. The effectiveness of dopamine re-uptake inhibitors in treating the symptoms of ADHD has led to the hypothesis that ADHD may arise from low tonic levels of dopamine (particularly in the fronto-limbic circuitry), but evidence in support of this theory is mixed. Genetics There are several difficulties when it comes to trying to identify a gene for complex traits such