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The **norepinephrine transporter** (NET) and **dopamine transporter** (DAT) are closely related members of the SLC6 family of sodium-chloride-dependent neurotransmitter transporters. NET (SLC6A2) is primarily responsible for the reuptake of norepinephrine from the synaptic cleft into noradrenergic neurons, thus terminating noradrenergic signaling[2][3]. DAT (SLC6A3) serves a similar role for dopamine in dopaminergic neurons[4][6]. Both proteins comprise twelve transmembrane helices and utilize sodium and chloride ion gradients to drive neurotransmitter uptake[1][2][4][6]. They are crucial for the regulation of mood, reward, attention, and autonomic function, and are targets for many antidepressants, ADHD medications, and drugs of abuse[3][4][5][6]. Alterations in NET or DAT function or expression are implicated in several neuropsychiatric and neurodegenerative diseases, and both transporters are of major therapeutic interest in neuropharmacology[3][6]. Note: Separate, structured records should ideally be created for each transporter with their specific gene/protein details and drug-interaction profiles.
Inhibitors block reuptake of norepinephrine (NET) or dopamine (DAT), increasing extracellular levels of these neurotransmitters in the synaptic cleft, which potentiates neurotransmission. Competitive inhibition at the primary substrate binding site (S1 site). Some compounds act as non-competitive or allosteric modulators.
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