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In rats, atomoxetine increased prefrontal cortex catecholamine concentrations without altering dopamine levels in the striatum or nucleus accumbens; in contrast, methylphenidate, a dopamine reuptake inhibitor, was found to increase prefrontal, striatal, and accumbal dopamine levels to the same degree.
Delayed onset of action. Is slightly-modestly less efficacious than methylphenidate and atomoxetine. [149] Buspirone: Buspar [150] Not available No No 5-HT 1A partial agonist: Low [c] Delayed onset of action. Being a 5-HT 1A receptor partial agonist may afford it the ability to increase dopamine release in the prefrontal cortex. [155] [156 ...
CYP2D6 inhibitors (e.g., fluoxetine, paroxetine and quinidine) can increase exposure for atomoxetine and it can also increase atomoxetine steady-state plasma concentration. Antihypertensive drugs because it can possibly increase the blood pressure; β2-agonist e.g. albuterol because it may increase the efficacy of albuterol on the ...
A dopamine reuptake inhibitor (DRI) is a class of drug which acts as a reuptake inhibitor of the monoamine neurotransmitter dopamine by blocking the action of the dopamine transporter (DAT). Reuptake inhibition is achieved when extracellular dopamine not absorbed by the postsynaptic neuron is blocked from re-entering the presynaptic neuron.
More specifically, it looked at the effect of methylphenidate (brand names Ritalin, Concerta), a stimulant, and atomoxetine (Strattera), a non-stimulant, on the brain.
[59]: 13 Atomoxetine alleviates ADHD symptoms through norepinephrine reuptake and by indirectly increasing dopamine in the pre-frontal cortex, [253] sharing 70-80% of the brain regions with stimulants in their produced effects. [252] Atomoxetine has been shown to significantly improve academic performance.
A monoamine reuptake inhibitor (MRI) [1] is a drug that acts as a reuptake inhibitor of one or more of the three major monoamine neurotransmitters serotonin, norepinephrine, and dopamine by blocking the action of one or more of the respective monoamine transporters (MATs), which include the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT).
The pharmacology of antidepressants is not entirely clear.. The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine). [1]