Influence of reduced serotonin on aggression and emotionality.

Abstract

Historically, theories on aggression only considered the impact of environmental, biological, and sociological factors. However, recent evidence suggests physiological sources of aggression deserve greater attention. One chemical imbalance in the body related to aggression and heightened reactivity involves the neurotransmitter serotonin, 5-HT. In humans, lower than normal amounts of 5-HT are related to violent behaviors, suicide, and depression. Nonhuman animals with low 5-HT levels show inhibited growth, heightened reactivity to stimuli, and increased attacking behavior towards other animals. The integral component in the relationship between low 5-HT and increased aggression and reactivity is the amino acid tryptophan which organisms normally receive through their diet. Because 5-HT is synthesized from tryptophan, the amount of brain serotonin is exclusively dependent upon the amount of available tryptophan. To test the low 5-HT-increased aggression and reactivity relationship, the present investigations evaluated levels of aggression and reactivity following exposure to two methods designed to reduce tryptophan transfer and 5-HT synthesis in rats. Reductions in 5-HT synthesis were accomplished in two ways. First, dietary intake of tryptophan was significantly limited by feeding rats a diet consisting only of com grits, a food containing minute amounts oftryptophan. In a second condition, the amount oftryptophan allowed to enter the brain was reduced. Animals received an aspartame-water mixture in addition to a the brain was reduced. Animals received an aspartame-water mixture in addition to a standard diet. Aspartame, more commonly known as Nutrasweet, blocks the transfer of tryptophan into the brain thereby reducing brain tryptophan levels and serotonin synthesis. Results supported the hypothesis that tryptophan-challenged rats would make longer and more numerous aggressive responses, and show stronger aversions to a novel flavor, than rats with no tryptophan deficiencies. Possible sources of this relationship and applicable conclusions are presented.