All three catecholamine systems—dopaminergic, adrenergic, and noradrenergic—are implicated in the pathophysiology of AD-HKD and its response to pharmacological treatment. Dysregulation of the central noradrenergic system may result in the inefficient priming of the cortex (i.e. quietening of activation in preparation for action). Dopaminergic mechanisms have a critical role in executive function processes; peripheral adrenaline may have a significant function in the therapeutic response to stimulant medication. (H9)
Stimulants are sympathomimetic amines that closely resemble neurotransmitters. Dextroamphetamine and methylphenidate are considered indirect catecholamine agonists. These stimulants facilitate the action of dopamine and noradrenaline agonists by inhibiting their reuptake, facilitating their release into the synaptic cleft, and inhibiting the catabolic activity of monoamine oxidase.(l20) Weak antagonism of the a2-adrenergic receptors may also contribute to the central effects of the amphetamine/121) Tricyclic antidepressants, which are also used in the treatment of AD-HKD, increase plasma noradrenaline by blocking its reuptake, but have virtually no effect on the dopaminergic system. This may explain why the primary impact of the tricyclic antidepressants is on the behavioural manifestations of AD-HKD and why these antidepressants are less beneficial for cognitive and academic functions.(l22)
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