Figure 6.

Under normal conditions, DA is converted into NE via DβH in vesicles of noradrenergic terminals. Following action potential stimulation substrate is released. DA and NE are transported back into the presynaptic terminal via NET and once intracellular into vesicles by VMAT2. In the presence of AMPH (AMPH is transported intracellularly into LC terminals by NET) VMAT2 function is prevented and MAO is blocked. The former action prevents concentration of DA in vesicles where DβH is located, preventing formation of NE and increasing intracellular concentrations of DA. Inhibition of MAO prevents the breakdown of DA to DOPAC, which further increases the intracellular concentration of DA. The increased cytosolic concentration of DA may result in reverse transport of DA to the extracellular media via NET down its concentration gradient where it interacts with D1Rs.