In previous papers we reported a deficit of tyrosine (TYR) and tryptophan (TRP) transport across the erythrocyte membrane in depressed patients. To investigate further the transport mechanism of both monoamine precursors, we tested in healthy subjects the role played by membrane fluidity, using different fluidizing agents such as alcohols and the neuroleptic chlorpromazine. We found that the transport of both amino acids depended on the length of the chain of each alcohol tested (number of carbon atoms = C). No inhibition was observed after methanol (C1) preincubation, in contrast to benzyl alcohol (C6), which produced an inhibition of about 80% of amino acid basal transport. In a condition of incubation by suspension of cells in an artificial medium, we observed a dose response of these transports with ethanol used at doses of 0.1–1.3 M. Finally we found in this study that the effect of ethanol on membrane fluidity, and therefore on inhibition of basal amino acid transport, was totally reversible after having washed the suspended cells, suggesting a superficial, noncovalent ethanol binding on such biological membrane