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    We are grateful to the Wellcome Trust for major financial support. The Mental Health Research Fund, the Science Research Council and St. Mary's Hospital Joint Standing Research Committee also gave generous support.


Crude mitochondrial fractions prepared from rat brains took up l-tryptophan. The component of the crude mitochondrial fraction responsible for this uptake is the synaptosome. After uptake of tryptophan occurred, rupture of synaptosomes released 97 per cent of the tryptophan unchanged. Rupture of synaptosomes abolished uptake.

Penetration of the limiting membrane of synaptosomes by l-tryptophan both as influx and efflux was studied. Uptake of l-tryptophan was rapid, temperature dependent, partially inhibited by cyanide, 2-deoxy-d-glucose and ouabain, but apparently unaffected by low external sodium ion concentrations. d-tryptophan was a poor inhibiteur of l-tryptophan uptake. Concentration gradients Internal: external of up to 4:1 were achieved. Kinetic studies on l-tryptophan uptake and its competitive inhibition by l-phenylalanine indicated a saturable carrier-mediated transport system, present in the rat at birth.

l-Tryptophan efflux from preloaded synaptosomes was markedly stimulated by certain arrino acids and its influx stimulated by preloading with l-tryptophan. This countertransport is further evidence for carrier-mediated or facilitated diffusion. On the basis of countertransport data there seem to be at least two systems for transporting amino acids across synaptosomal membrane.

The relevance of these studies to the role of l-tryptophan as the initial precursor of brain 5-hydroxytryptamine is examined.