PubMed · 10238792
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1978-09-15. Dealing with aggressive behavior.. https://pubmed.ncbi.nlm.nih.gov/10238792/
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OBJECTIVE: To evaluate the effect of high- and low-protein diets with or without tryptophan supplementation on behavior of dogs with dominance aggression, territorial aggression, and hyperactivity. DESIGN: Prospective crossover study. ANIMALS: 11 dogs with dominance aggression, 11 dogs with territorial aggression, and 11 dogs with hyperactivity. PROCEDURE: In each group, 4 diets were fed for 1 weeks each in random order with a transition period of not < 3 days between each diet. Two diets had low protein content (approximately 18%), and 2 diets had high protein content (approximately 30%). Two of the diets (1 low-protein and 1 high-protein) were supplemented with tryptophan. Owners scored their dog's behavior daily by use of customized behavioral score sheets. Mean weekly values of 5 behavioral measures and serum concentrations of serotonin and tryptophan were determined at the end of each dietary period. RESULTS: For dominance aggression, behavioral scores were highest in dogs fed unsupplemented high-protein rations. For territorial aggression, [corrected] tryptophan-supplemented low-protein diets were associated with significantly lower behavioral scores than low-protein diets without tryptophan supplements. CONCLUSIONS AND CLINICAL RELEVANCE: For dogs with dominance aggression, the addition of tryptophan to high-protein diets or change to a low-protein diet may reduce aggression. For dogs with territorial aggression, tryptophan supplementation of a low-protein diet may be helpful in reducing aggression.
Ethanol may modulate the activity of presynaptic terminals to increase extracellular dopamine release in the nucleus accumbens though conflicting results have been published. It has been suggested that the stress of social defeat might be a factor influencing the effects of ethanol. We investigated the effects of ethanol on the evoked dopamine overflow in the nucleus accumbens in anaesthetised mice by in vivo voltammetry. Dominant animals, subordinates which had been defeated following eight intruder-resident encounters, and subordinate nondefeated mice were used. The overflow was evoked by electrical stimulation of the median forebrain bundle (100 pulses) at low (20 Hz) and high (50 Hz) frequencies of stimulation. Ethanol at 0.1 and 2 g/kg had no effects on evoked dopamine overflow in aggressive and nondefeated mice. Ethanol increased dopamine release at 0.1 g/kg and decreased release at 2 g/kg following high frequency stimulation in defeated mice. These data suggest that the stress of social defeat may have sensitised the machinery involved in dopamine release to ethanol, a process that may increase the reinforcing properties of this compound.
The aim of this study was to investigate the monoamine content in post-mortem brain samples of control, apomorphine-aggressive, and apomorphine-non-aggressive adult male Wistar rats. The repeated apomorphine (1.0 mg/kg, (s.c.) once daily during 2 weeks) gradually induced aggressive behaviour in 18 animals out of 24. No unidirectional changes in the brain monoamine contents in four regions (frontal cortex, striatum, hippocampus, and hypothalamus) were detected as measured by high pressure liquid chromatography-electrochemical detection. In conclusion, our present experiment demonstrates that the development and intensity of apomorphine-induced aggressive behaviour do not correlate with the brain post-mortem monoamine content.