In addition to an interaction with the TBZ/DTBZOH binding site, some propose that substituted amphetamines like methamphetamine decrease dopamine uptake because of the weak base properties of substituted amphetamines. This “Weak Base Hypothesis” proposes that amphetamine analogs enters the cell through transport and lipophilic diffusion then likewise diffuses through the vesicular membrane where it accumulates in synaptic vesicles and offsets the proton electrochemical gradient in the vesicle that drives monoamine transport through VMAT. In this way, amphetamine administration would prevent vesicular DA uptake through VMAT, and explain the finding that amphetamine administration correlates with decreased dopamine release from vesicles and a neurotoxic increase in intracellular dopamine.