for the control of movement; the degeneration of dopamine-using neurons in a portion of the midbrain leads to Parkinson's disease. A patient with this condition finds it difficult to initiate movement and also to stop, and to manage associated actions such as swinging the arms while walking. A slow tremor of the hands and head, present when the patient is at rest but not during movement, is probably what gave the illness its original name of “the shaking palsy.” Although the progress of the disease cannot be halted, the symptoms of Parkinson's disease can be effectively controlled in most patients by treatment with L-dopa. (This is not the actual transmitter itself but a precursor, a molecule that has the ability to pass through the blood-brain barrier and from which the brain can form dopamine.)
Because dopaminergic neurons are also well distributed in the limbic system, we would expect some role for this neurotransmitter in the creation of mood—and, indeed, evidence to this effect is accumulating. Most striking are the signs that a relative increase in dopamine activity in the frontal cortex may provide the biochemical basis for schizophrenia.
Evidence for the role of dopamine has come from several directions. Chlorpromazine, a drug first used widely in mental hospitals in the 1950s and 1960s to reduce the overt symptoms of schizophrenia, was found in the 1970s to block the action of dopamine at receptor sites. Then, too, some of the patients who were given the medication to help control their hallucinations and thought disorders developed, over the long term, a tremor and other physical symptoms that resembled those of Parkinson's disease. A third clue may be the ability of amphetamines, when taken in sufficient quantity, to bring on disturbances of the mind much like schizophrenia; it is known that amphetamines, or “uppers,” increase the levels of dopamine available in the brain.
To be sure, an illness as complex as schizophrenia cannot be reduced to a simple chemical explanation such as “excess of dopamine.” The question remains open whether the schizophrenic brain suffers from too much dopamine, too many dopamine receptors, a standard quantity of receptors with abnormally high sensitivity, or some other dysfunction entirely—to say nothing of the important genetic, social, and psychological factors also under study. Science has a long way to go yet in