A noradrenaline reuptake inhibitor (NRI), is a type of drug that blocks the action of the norepinephrine transporter (NET). And NRI can increase adrenergic neurotransmission. Furthermore, NRIs have psychostimulatory effects and are therefore often used in the study of disorders such as attention-deficit hyperactivity disorder (ADHD) and narcolepsy. ADHD is the most common neurodevelopmental disorder characterized by inattention, impulsivity, and hyperactivity. Although ADHD shows a high prevalence, its underlying neuropathological mechanisms are still unclear. Additionally, there is concern that long-term treatment with these drugs, which act predominantly on the dopaminergic and noradrenergic systems, could be detrimental.

Atomoxetine (also known as Tomoxetine or LY 139603) is a selective noradrenaline reuptake inhibitor with Ki values of 5, 77 and 1451 nM for norepinephrine (NE), serotonin (5-HT), and dopamine (DA) transporters, respectively. In microdialysis studies, Atomoxetine increases extracellular levels of norepinephrine in the prefrontal cortex (PFC) 3-fold, but does not alter 5-HT extracellular levels. This compound can enhance catecholaminergic neurotransmission in PFC. More importantly, Atomoxetine has the potential for attention-deficit hyperactivity disorder (ADHD) research. In fact, Atomoxetine Atomoxetine effectively improves behaviors associated with ADHD in rats at intraperitoneal doses as low as 0.1 mg/kg. For example, Cain et al. found that improvement in attentional set shifting in adult Long Evans rats following intraperitoneal injections of 0.1 mg/kg Atomoxetine. In addition, Atomoxetine does not increase dopamine in striatum or nucleus accumbens. Thereby it would not have motoric or drug abuse liabilities. Furthermore, Atomoxetine also potently blocks Na⁺ channels (VGSCs).

To sum up, Atomoxetine is a selective noradrenaline reuptake inhibitor that relieves the symptoms of attention-deficit hyperactivity disorder (ADHD).

References:

[1] Turner M, et, al. Behav Brain Res. 2013 Apr 15;243:28-37.

[2] Bymaster FP, et, al. Neuropsychopharmacology. 2002 Nov;27(5):699-711.