Dopamine is the critical neurotransmitter for reward. Cocaine administration increases metabolism in the substantia nigra (SN), which can explain the altered motor function seen in cocaine-using subjects. However, cocaine is even more active in the dopaminergic neurons of the ventral tegmental area (VTA) than the substantia nigra. (Joan M. Lakoski, Joan M., et al. Cocaine. Telford Press, 1991.)
Cocaine impacts the human brain in several ways, one of which involves the inhibition of dopamine reuptake. Interference with dopamine reuptake explains cocaine's addictive properties, as dopamine is the critical neurotransmitter for reward. (Heikkila, R E; et al. Motor activity and rotational behavior after analogs of cocaine: correlation with dopamine uptake blockade. Commun Psychopharmacol 3 (5): 285–90. 1979.)
Studies: Cocaine-exposed babies show signs of addiction at birth. As with prenatal exposure to alcohol, these babies have a lower birth weight, are shorter, and have a smaller head. They cry, often piercingly, shake, show erratic sleep-wake cycles, have trouble feeding, and are difficult to comfort. (Karr-Morse, Robin, and Meredith S. Wiley. Ghosts from the Nursery, Tracing the Roots of Violence. NY: Atlantic Monthly Press, 1997, pp 72-73)
Refer to Substances and the Brain for additional information.