Pharmacological control of aggressive behavior in mice.
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Biomedical subjects
Publications and source records attributed to L Valzelli.
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During aging, male Sprague-Dawley rats display increasing frequency of bursts of seizure-like EEG patterns. They also have a decreased retention of passive avoidance response and a loss of spontaneous alternation in a Y maze. A study was made on the effects of chronic administration of phosphatidylserine in aged rats. It was found that BC-PS reduced by 65% the number of seizures, and by 70% their duration. It also facilitated retention of passive avoidance and of spontaneous alteration behavior. These results suggest that phosphatidylserine can affect electrophysiological and behavioral parameters in aged rats probably by counteracting age-related biochemical changes.
Male Wistar rats were given orally for seven days water, clonidine (0.125 or 0.25 mg/kg bid) or S3341, a new clonidine-like drug (2.5 or 5.0 mg/kg bid) and afterwards pairs of rats were injected ip with 2.5 mg/kg of apomorphine (APO). Water-treated animals did not behave aggressively. Clonidine and S3341 both induced clear aggression when combined with a subthreshold dose of APO. Some degree of hyperirritability developed in these two groups during drug treatment when observed in the home-cage. No significant changes in aggressive behavior were noted upon acute administration of both drugs, though some tendency to augment aggressivity could be observed after clonidine (0.25 mg/kg po). It is suggested that noradrenergic neurons play an inhibitory role in APO-induced fighting.
Bilateral lesions of basomedial amygdaloid nuclei are capable of significantly inhibiting muricidal aggression induced by oral p-chlorophenylalanine (p-CPA) in male rats. Rats lesioned in extra-amygdaloid structures or sham-lesioned show the usual p-CPA-induced muricidal activity, which ranges from 70 to 80% of treated animals. The results obtained indicate that basomedial amygdaloid nuclei play an important role in regulating p-CPA-induced muricidal aggression, even though the effect lasts for a relatively limited period of time. This fact is probably due to the intervention of still unidentified compensatory mechanisms.
The role played by the inhibitory control of brain functions appears reportedly essential in the regulation of emotions and behavior, and is of great relevance in explaining the behavioral changes that follow induced or spontaneous impairment of the serotonergic system of the brain. As a matter of fact, numerous evidence indicate that genetic predisposition and induced or acquired defects of serotonergic inhibitory control greatly concur to precipitate anomalous strong aggression. The cluster of symptoms presented by laboratory rats in consequence of the serotonergic discontrol confers to laboratory experiments the value of a tool aimed at a better understanding of the biological mechanisms which underlie pathological aggression and violence.