Latest research on Atomoxetine

Atomoxetine is the first non-stimulant drug approved for the treatment of attention-deficit hyperactivity disorder (ADHD). It is sold in the form of the hydrochloride salt of atomoxetine. This chemical is manufactured and marketed under the brand name Strattera; by Eli Lilly and Company and as a generic Attentin by Torrent Pharmaceuticals. There is currently no generic available within the United States due to patent restrictions. [Wikipedia]

Atomoxetine side effects

The selective Norepinephrine reuptake inhibitor Atomoxetine increases the amount of Norepinephrine available in the synapse by preventing its reuptake by the presynaptic terminals. [source, 2015]
Therefore, passive emergence after a single IV dose of Propofol can be used to test for arousal changes induced by Dextroamphetamine or Atomoxetine, because changes in respiratory drive will not confound the results. [source, 2015]
In the Atomoxetine group, mean time to emergence was 566 sec (95% CI: 468 to 678 sec, n = 8) but this decrease in comparison to the normal saline group was not statistically significant (mean difference: 75 sec; 95% CI: -82 to 228 sec). [source, 2015]
Similar to Dextroamphetamine, the administration of Atomoxetine (3 mg/kg IV) rapidly decreased the amplitude and increased the frequency of the EEG waveform. [source, 2015]
The group power spectral density from all three rats (Fig 5C) shows that Atomoxetine induced a statistically significant decrease in power at most frequencies below 10 Hz, and shifted peak power from δ to θ. [source, 2015]
Dextroamphetamine causes the release of Dopamine and Norepinephrine from presynaptic terminals, whereas Atomoxetine is a reuptake inhibitor that is approximately 1000 times more selective for NET than DAT [18]. [source, 2015]
Because Atomoxetine is highly selective for NET over DAT [18], the present results suggest that noradrenergic stimulation alone is insufficient to induce reanimation from general anesthesia. [source, 2015]
Indeed, this dose of Atomoxetine was high enough to cause significant EEG changes during general anesthesia in the present study, indicating that a sufficient quantity of the drug had reached the brain to induce neurophysiological changes. [source, 2015]
Because Methylphenidate, Dextroamphetamine and Atomoxetine all enhance noradrenergic neurotransmission [18], the present results are consistent with the notion that noradrenergic stimulation during general anesthesia induces a shift in EEG peak power from δ to θ. [source, 2015]
Interestingly, it has been reported that Atomoxetine increases not only extracellular Norepinephrine levels, but also Dopamine levels in the prefrontal cortex [36]. [source, 2015]