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Effects on striatal dopamine

While caffeine does not directly bind to any dopamine receptors, it influences the binding activity of dopamine at its receptors in the striatum by binding to adenosine receptors that have formed GPCR heteromers with dopamine receptors, specifically the A – D receptor heterodimer (this is a receptor complex with one adenosine A receptor and one dopamine D receptor) and the A – D receptor heterotetramer (this is a receptor complex with two adenosine A receptors and two dopamine D receptors). The A –D receptor heterotetramer has been identified as a primary pharmacological target of caffeine, primarily because it mediates some of its psychostimulant effects and its pharmacodynamic interactions with dopaminergic psychostimulants.

Caffeine also causes the release of dopamine in the dorsal striatum and nucleus accumbens core (a substructure within the ventral striatum), but not the nucleus accumbens shell, by antagonizing A receptors in the axon terminal of dopamine neurons and A – A heterodimers (a receptor complex composed of one adenosine A receptor and one adenosine A receptor) in the axon terminal of glutamate neurons. During chronic caffeine use, caffeine-induced dopamine release within the nucleus accumbens core is markedly reduced due to drug tolerance.