Abstract
It has been established that the selective α2A adrenoceptor agonist guanfacine re‐duces hyperactivity and improves cognitive impairment in patients with attention‐deficit/hyperactivity disorder (ADHD) . The major mechanisms of guanfacine are considered to be involved in the activation of the postsynaptic α2A adrenoceptor of glutamatergic pyramidal neurons in the orbitofrontal cortex, but the effects of chronic guanfacine administration on catecholaminergic and glutamatergic transmissions in the orbitofrontal cortex remained to be clarified. Therefore, the present report discussed with pathophysiology of ADHD via effects of selective α2A adrenoceptor agonist, guanfacine, on noradrenergic, GABAergic and glutamatergic transmission.
