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A serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI), also known as a triple reuptake inhibitor (TRI), is a type of drug that acts as a combined reuptake inhibitor of the monoamine neurotransmitters serotonin, norepinephrine, and dopamine.
Symptoms may occur because concentrations of neurotransmitters, such as norepinephrine and serotonin, are insufficient, leading to downstream changes. [10] [25] Medications for depression affect the transmission of serotonin, norepinephrine, and dopamine. [10]
The skeletal structure of norepinephrine The skeletal structure of dopamine. A norepinephrine–dopamine reuptake inhibitor (NDRI) is a drug used for the treatment of clinical depression, attention deficit hyperactivity disorder (ADHD), narcolepsy, and the management of Parkinson's disease.
α-Methyltryptamine [αMT] (Indopan) – non-selective serotonin receptor agonist, serotonin–norepinephrine–dopamine releasing agent (SNDRA), and weak RIMA Etryptamine [α-Ethyltryptamine (αET)] (Monase) – non-selective serotonin receptor agonist, SNDRA, and weak RIMA
The entactogen MDMA is a serotonin releasing agent and, while it also possesses other actions such as concomitant release of norepinephrine and dopamine and weak direct agonism of the serotonin 5-HT 2 receptors, its serotonin release plays a key role in its unique entactogenic effects. [141]
Amphetamine, for example, is a stimulant that increases release of norepinephrine as well as dopamine. [53] Monoamine oxidase A inhibitors (MAO-A) are antidepressants that inhibit the metabolic degradation of norepinephrine as well as serotonin and dopamine. [54]
Cocaine is a nonselective, reuptake inhibitor of the norepinephrine, serotonin, and dopamine transporters. This thwarts the absorption of these chemicals into the presynaptic terminal [ 27 ] and allows a large concentration of dopamine, serotonin and norepinephrine to build up in the synaptic cleft.
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]