Attention Deficit Hyperactivity Disorder (ADHD) is one of the most prevalent child hood developmental disorder affecting children. Nearly 11% of children ages 4-17 were diagnosed with ADHD (data from CDC, 2011). Dopamine plays important role as a neurotransmitter in brain and is linked to motor function, reward and cognition. ADHD is characterized by age inappropriate symptoms of inattentiveness, impulsiveness and hyperactivity in children affected, this condition can persist into adulthood, in fact 65% of kids affected, have ADHD in adulthood. Neurotransmitter dopamine has central role in regulations of above psychomotor activity, motivation, and attention. Animal model studies on ADHD (using the Spontaneously hypertensive rats – model for ADHD ) show the downregulation of dopaminergic neurotransmission in the brain. In ADHD the focus has been on blocking striatal dopamine transporter, which can thus lead to enhanced dopamine availability. Drugs such as methylphenidate increase the synaptic concentration of dopamine by blocking the presynaptic re-uptake of Dopamine.
Methylphenidate is classified as as a central nervous system stimulant, it is also used in treating narcolepsy (disorder with excessive daytime sleepiness). It works as a dopamine reuptake inhibitor by blocking the DAT and leading to increased concentration of dopamine in synaptic cleft allowing the increased neurotransmission of dopamine. Oroxylin A, naturally occurring flavonoid present in plants like Scutellaria baicalensis, Oroxylum indicum has similar activity as methylphenitade. In animal models, Oroxylin A alleviated the symptoms of ADHD such as hyperactivity, impulsivity and inattention and also had awakening effect. In vitro studies carried out on Oroxylin A showed that Oroxylin A inhibited the Dopamine uptake in similar fashion as methylphenitade but did not influenced norepinephrine uptake. Methylphenidate while alleviating the impulsivity and inattentiveness did not effect the hyperactivity. These findings show that Oroxylin A can improve ADHD like behavior via enhancement of dopamine transportation and not modulating the GABA pathway Seo et al 2008).