dopamine
Dopamine is a brain chemical with several day jobs at once. In one set of pathways it lets you move smoothly; in another it flags rewarding events and drives motivation; in yet another it shapes thought and emotion. Because it wears so many hats, drugs that touch dopamine ripple across movement, mood, and psychosis all together.
Dopamine is a catecholamine neurotransmitter acting on dopamine receptors (D1-like and D2-like, all G-protein-coupled). Its major brain circuits are the nigrostriatal pathway (movement), the mesolimbic and mesocortical pathways (reward, motivation, cognition), and the tuberoinfundibular pathway (which suppresses prolactin release). Different diseases and drugs hit different circuits.
This anatomy explains key drugs: loss of nigrostriatal dopamine causes Parkinson's disease, treated by raising dopamine with levodopa; excess mesolimbic dopamine signalling is linked to psychosis, treated by blocking D2 receptors with antipsychotics; and dopamine's role in reward underlies the pull of addictive drugs.
The catch is that no drug can target one pathway in isolation. Boosting dopamine for Parkinson's can cause psychosis or impulse-control problems, while blocking it for psychosis can cause parkinsonism and raise prolactin — the two therapies are mirror images of one another.
The opposite directions of dopamine therapy are striking: an antipsychotic that blocks D2 receptors can cause Parkinson-like stiffness, the very symptom that levodopa, which raises dopamine, is given to relieve.
Raising versus blocking dopamine are mirror-image therapies.
Dopamine itself is sometimes given intravenously as a drug to support blood pressure and the failing heart, but it does not cross the blood–brain barrier, which is exactly why Parkinson's is treated with levodopa instead.