Muricidal Aggression Research Articles

Effect of haloperidol on extracellular concentrations of dopamine and its metabolites in the rat septum during muricidal aggression

Effect of haloperidol on extracellular concentrations of dopamine and its metabolites in the rat septum during muricidal aggression

Anxiolytic activity on locus coeruleus-mediated suppression of muricidal aggression

The evidence suggests that stimulation of brain noradrenergic neurons plays an inhibitory role in rat mouse-killing (muricidal) aggression. Anxiolytic benzodiazepines inhibit locus coeruleus activity and previous data showed that chlordiazepoxide was capable of antagonizing the locus coeruleus-mediated suppression of muricidal aggression. The present experiments showed that this effect is common to new anxiolytic triazolobenzodiazepines and to other non-benzodiazepine derivatives with anxiolytic activity. In this framework, 10 mg/kg of buspirone, of 1-pyrimidine-piperazine and of MJ-13805 proved to be as active as 2.5 mg/kg of alprazolam and as 5 mg/kg of chlordiazepoxide in inhibiting the locus coeruleus-mediated suppression of muricidal aggression.

Activity of desipramine, fluoxetine and nomifensine on spontaneous and P-CPA-induced muricidal aggression

Antidepressant drugs reportedly counteract mouse-killing activity by rats. There is evidence that antidepressant derivatives exert their anti-muricidal activity through both noradrenergic and serotonergic neurons. The experiments were performed in two types of muricidal aggression with three antidepressants characterized by different neurochemical activity. No major differences in the antimuricidal efficacy of the drug-employed were found, even though spontaneous muricidal animals resulted on the whole less sensitive to antidepressants than p-CPA-induced muricidal rats. In these last animals nomifensine proved to be more potent than desipramine and fluoxetine.

The pain threshold increasing effects by thiamine deficiency in rats.

It is well known that rats maintained on a thiamine deficient diet exhibit significant weight loss, decrease in heart frequency, behavioral disorders such as circling movements, muricide aggression as well as symptoms of polyneuritis. After a series of pharmacological studies on thiamine deficient rats, I reported that the actions of certain drugs affecting the central nervous system were modified by acute thiamine deficiency in animals. In brief, thiamine deficiency increased sensitivity to the hypnotic action of barbiturates and reduced the cataleptic action by tetrabenazine4). I am planning to investigate the effect of analgesics (morphine, pentazocine, aspirin……) on thiamine deficient animals, since little is known about changes in the pain threshold following severe thiamine deficiency. In this study, an attempt was made to investigate the changes in the pain threshold of rats as a consequence of thiamine deficiency.

Time-courses of P-CPA-induced depletion of brain serotonin and muricidal aggression in the rat

p-Chlorophenylalanine is known to selectively decrease brain serotonin and to induce muricidal aggression in previously docile rats. With regard to the substance's relatively time-limited effect on brain serotonergic system, the neurochemical activity of p-CPA on tryptophan, serotonin and 5-hydroxyindoleacetic acid on seven discrete areas of the rat brain is studied in parallel to the time-course of muricidal aggression induced by the drug. Evidence indicates that, following the disruption of brain serotonergic inhibitory control, muricidal aggression becomes a stable behavior, probably on account of its self-reinforcing property.

Fluoxetine activity on muricidal aggression induced in rats by p-chlorophenylalanine

Fluoxetine activity on muricidal aggression induced in rats by p-chlorophenylalanine

Characteristics of muricide induced by thiamine deficiency and its suppression by antidepressants or intraventricular serotonin

Male Wistar rats maintained on a thiamine deficient diet showed muricide aggression. On the 30th day of experimental feeding, the incidence was 70% and the killing latency was very short in the thiamine deficient killer-rats. They did not kill their rat-pups. Intraventricular injection of serotonin (5-HT) was effective in suppressing the muricide induced by thiamine deficiency. The suppressive effect of 5-HT was strongly antagonized by antiserotonergic agents, morphine and chlorpromazine. Moreover, the suppressive effect of 5-HT was potentiated by iproniazid, a monoamine oxidase inhibitor. Various antidepressants had suppressive effects on this muricide to varying degrees. Muricide induced by thiamine deficiency was more potently suppressed by the tricyclic antidepressants which inhibit 5-HT uptake rather than noradrenaline uptake. Our results in these experiments strengthened the hypothesis that central serotonergic neurons are involved in the inhibition of the muricide aggression in thiamine deficient killer-rats.

Effect of tryptophan administration on spontaneous and p-CPA-induced muricidal aggression in laboratory rats

Summary Muricidal activity, by which some strains of rats stereotypically kill mice, can be induced in laboratory rats by surgical, pharmacological or environmental manipulations, which consistently impair serotonergic transmission in the brain of treated animals in a variety of ways. Manipulations of tryptophan intake result in either facilitation or reduction of spontaneous muricidal activity in rats. In this framework, p-CPA inducesmuricidal activity in naive laboratory rats, even against any genetic predisposition, and orally-administered 1-tryptophan is shown to inhibit p-CPA-induced muricidal aggression.