Opioid substances mimic the effects of endogenous opioids within the brain, binding to opioid receptors.1
Stimulants directly increase dopamine transmission in the nucleus accumbens. Opiates indirectly increase dopamine transmission by inhibiting GABAergic interneurons in the ventral tegmental area, which disinhibits the dopaminergic neurons and allows dopamine signalling to occur.
Both routes converge on the dopaminergic reward pathway implicated in substance use disorders.