Short answers, pulled from the story.
A single dopamine molecule consists of a benzene ring with two hydroxyl side groups and one amine group attached via an ethyl chain. This structure makes it the simplest possible catecholamine, a family that also includes norepinephrine and epinephrine.
George Barger and James Ewens first synthesized dopamine in 1910 at Wellcome Laboratories located in London England. Katharine Montagu identified dopamine in the human brain for the first time in 1957 giving it its current name derived from its precursor L-DOPA.
Outside the central nervous system dopamine functions primarily as a local paracrine messenger affecting organs like the kidneys and immune system. In blood vessels it inhibits norepinephrine release and acts as a vasodilator to regulate flow while increasing sodium excretion to help prevent high blood pressure.
Cocaine blocks dopamine transporters preventing reuptake and resulting in increased concentrations within the synaptic cleft. Substituted amphetamines increase concentration through different mechanisms yet achieve similar outcomes regarding reward system activation.
The most widely used treatment involves administration of L-DOPA which serves as the metabolic precursor for dopamine. Unlike dopamine itself L-DOPA can cross the blood-brain barrier to reach neurons that have lost their ability to produce neurotransmitters.