Corticosteroid response to stress depends upon increased tryptophan availability.

Prior administration of valine to rats has been shown previously to prevent restraint stress-induced increases in brain tryptophan and 5HT turnover. The present study demonstrates that the accompanying attenuation of the corticosteroid response to this stress is substantially reversed by administration of tryptophan with the valine. Tyrosine is not effective in reversing this attenuation, and in fact itself attenuates the corticosteroid response to the stress when given alone. It is concluded that at least part of the corticosteroid response to restraint stress is mediated by an increase in serotonergic activity that is dependent on increased supply of the precursor, tryptophan, and that this can be antagonised by either of two amino acids which compete with tryptophan for access to the brain. Implications for stress-associated human disorders are discussed.