At the end of 1959, it was while preparing a review on monoamine oxidase inhibitors (MAOIs) at the Faculty of Pharmacy, that I discovered the early development of modern neuropharmacology, which started around 1955. Surprised by the sedative properties of chlorpromazine in patients recovering from surgery, Henri Laborit suggested that Jean Delay and Pierre Deniker use the new compound in schizophrenic patients. It was also at this time that the antidepressant properties of MAOIs were observed in patients treated for tuberculosis. The research then into neurotransmission was mainly performed on peripheral cholinergic and noradrenergic neurons, and almost nothing was known of brain neurotransmission. Then, in 1957, Marthe Vogt reported that noradrenaline levels were decreased in the hypothalamus of rats injected with morphine. That same year, Arvid Carlsson and his colleagues described the presence of large amounts of dopamine in the rat striatum and suggested that this catecholamine was not only the precursor of noradrenaline, but could also act as well as a neurotransmitter in some central neurons. Shortly thereafter, these researchers reported that homovanillic acid, the main dopamine metabolite, was markedly increased in the striatum of rats treated with chlopromazine. This led them to propose that this neuroleptic was blocking dopamine receptors, a remarkable hypothesis that was later confirmed. These authors also indicated that dihydroxyphenylalanine (DOPA) and 5-hydroxytryptophan, the respective precursors of dopamine and serotonin, were able to reverse the parkinsonism-like syndrome due to reserpine in rabbits. These striking findings of the Swedish researchers, and the elegant metabolic studies of Julius Axelrod and Georg Hertting on peripheral noradrenergic neurons, performed thanks to the use of radioactive noradrenaline, were responsible for my own project when I started my PhD thesis in 1960 at the Pasteur Institute. The goal was to prepare radioactive dopamine from carbon-14-labelled tyrosine and to study its metabolism following its intraventricular injection into the rat brain. My interest in dopamine research was reinforced by the recent studies of Oleh Hornykiewicz and colleagues in Vienna, who observed, on autopsy, that dopamine levels were markedly reduced in the pars compacta, caudate nucleus and putamen of parkinsonian patients. These authors were also responsible for the introduction of L-DOPA treatment for Parkinson's disease, which was rapidly taken up by Andre Barbeau in Quebec. Rapid progress was being made in dopamine synthesis, storage and turnover in the rat striatum from 1963 to 1966, when I joined Axelrod's team at the US National Institutes of Health in Bethesda, Maryland. The field was markedly accelerated by the histochemical report by Kjell Fuxe and Annika Dahlstrom in 1964, which described, for the first time, the mapping of the central dopaminergic neurons as well as other aminergic neurons.