Little is known about the psychobehavioral consequences of a dietary deficiency of the amino acid, L-lysine. This report demonstrates that a 4-d long L-lysine deficiency in rats interfered with the normal circadian release of the neurotransmitter serotonin, but not dopamine, measured by in vivo microdialysis in the central nucleus of the amygdala. L-Lysine deficiency was induced by feeding rats a L-lysine-deficient diet. Controls were pair-fed a L-lysine-sufficient diet. Footshock stress-induced anxiety, measured in an elevated plus-maze paradigm, and wrap-restraint stress-stimulated fecal excretion were significantly greater in the L-lysine-deficient rats than in the controls. We conclude that a severe deficiency of dietary L-lysine enhances serotonin release in the amygdala, with subsequent changes in psychobehavioral responses to stress.

No abstract

In this article we discuss studies showing that rats are able to regulate their intake of BCAA depending on the level of exercise, and that they will choose a solution of BCAA over water during times of intense exercise. We found that the voluntary intake of a solution made of BCAA, L-arginine and L-glutamine positively correlated with the timing and volume of exercise during the dark (active) period of the circadian rhythm. In the second behavioral protocol in which rats were fed BCAA fortified diet (2.0%, wt:wt), we observed voluntarily increased volume of physical activity beginning from d 4 of feeding on. In the second, neuro-behavioral, part of the study we measured the brain content of 5-hydroxytryptamine (5-HT) as well as plasma amino acid profiles in well-trained exercising rats to test a hypothesis that BCAA may alleviate central aspects of fatigue. A solution made of BCAA, L-arginine, and L-glutamine applied before running elevated the BCAA/tryptophan plasma ratio at the end of and after running, and decreased 5-HT release in the lateral hypothalamus and amygdala after running, when compared with the controls. The exercise-related shift in the fluid preference toward a BCAA-based solution suggests an ergogenic benefit. The forced-running study shows the lateral hypothalamus and possibly amygdala might be the critical brain regions implied in the central effects of a BCAA-based solution.

Rats were given free access to a running wheel, food, water, and a solution composed of branched-chain amino acids plus glutamine and arginine (the "BCAA-based" solution). A positive relationship between dark-period running distance and preference for the BCAA-based solution was observed. Serotonin release in the lateral hypothalamus, the central nucleus of amygdala and the medial nucleus raphe in overnight fluid-deprived rats during their first subsequent free drinking was also measured. A lowered serotonin release in the lateral hypothalamus characterized the rats that consumed the BCAA-based solution. No drink-related changes were observed in the amygdala. A separate group of rats was trained on a treadmill. Following the training period, plasma amino acids and brain serotonin release were measured during running. The BCAA-based solution infused before running elevated the branched chain amino acids/tryptophan plasma ratio at the end of, and after, running. Additionally, a decreased lateral hypothalamus serotonin release was seen 80 min after running, when compared with water-infused rats. No fluid-related changes in the amygdala were observed. The exercise-related shift in the fluid preference towards a BCAA-based solution suggests an ergogenic benefit. The forced-running study shows the lateral hypothalamus as a critical region in the effects of a BCAA-based solution.

Taste acceptance involves both innate and acquired components. We observed an increased acceptance of salty and sweet solutions in adult rats whose tongues had been exposed to an NaCl-enriched milk formula during one day of early postnatal development. This behavioral effect was associated with changes in the norepinephrine system of the basolateral amygdala. No other changes in behavior, food intake, body weight, blood or metabolic parameters of the NaCl-exposed adult rats were identified. The data suggest a causal relationship between NaCl taste exposure, low content of amygdala norepinephrine cells and enhanced intake of sweet and salty compounds by adult rats. They also raise the question of the extent to which similar phenomena may occur during early human infant feeding.