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Naltrexone, used for alcohol use disorder, blocks opioid receptors but also modulates dopamine release indirectly
This results from a tyramine-induced depletion of norepinephrine normally present in the readily releasable vesicle pool, and replacement of vesicular norepinephrine with tyramine (which functions as a false- or pseudo- neurotransmitter), which when released has no effect on postsynaptic adrenergic receptors (Figure 1)
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