In 1951, Carlsson became an associate professor at Lund University. He spent five months as a research fellow for the pharmacologist
Bernard Beryl Brodie at the
National Heart Institute in
Bethesda, Maryland, United States, and the change in his research focus to
psychopharmacology eventually led to his Nobel Prize. Carlsson went on to develop a method for measuring the amount of dopamine in brain tissues. He found that dopamine levels in the
basal ganglia, a brain area important for movement, were particularly high. He then showed that giving animals the drug
reserpine caused a decrease in dopamine levels and a loss of movement control. These effects were similar to the symptoms of Parkinson's disease. By administering to these animals
L-Dopa, which is the precursor of dopamine, he could alleviate the symptoms. These findings led other doctors to try using L-Dopa in patients with Parkinson's disease, and it was found to alleviate some of the symptoms in the early stages of the disease. L-Dopa is still the basis for most commonly used means of treating Parkinson's disease. He and his colleagues were able to
derive the first marketed
selective serotonin reuptake inhibitor (SSRI),
zimelidine, from
brompheniramine. but Carlson's research paved the way for
fluoxetine (Prozac), one of the most widely used prescription medicines in the world. on
OSU6162, a dopamine stabilizer which alleviates symptoms of post-stroke fatigue. == Honours and awards ==