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Injected tryptophan increases brain but not plasma tryptophan levels more in restrained rats.

Immobilization stress given for one hour decreased cumulative food intake and growth rate in rats. Activity in an open field scored next day was also smaller in the restrained animals. Stress is known to enhance brain serotonin (5-hydroxytryptamine; 5-HT) metabolism. It is however not clear, whether this enhancement is caused by an increase in the activity of tryptophan hydroxylase, the rate limiting enzyme of 5-HT biosynthesis or availability of the precursor tryptophan to the brain. In order to determine the utilization of tryptophan via serotonin path way in brain during stress; rats were injected with saline or tryptophan (50 mg/kg, i.p.). A group of both saline and tryptophan injected animals was restrained for one hour, while another group left unrestrained. The animals were killed immediately after the termination of stress period to collect plasma and brain samples. Injected tryptophan resulted in 3-4 fold rise of plasma tryptophan in both unstressed and stressed animals in one hour. Stress alone however had no effect on plasma total tryptophan concentration. Free tryptophan in plasma, brain tryptophan, 5-HT and 5-hydroxyindole acetic acid (5-HIAA) all increased by both stress and tryptophan injection. The increases of brain tryptophan, 5-HT and 5-HIAA but not of free tryptophan in plasma were considerably greater in restrained animals given tryptophan load. The results suggest that enhancement of brain serotonin metabolism during stress is caused by an increase in the availability of tryptophan to the brain as well as an increase in the activity of the enzyme tryptophan hydroxylase. Factors affecting the availability of tryptophan to the brain are discussed.