Mouse-killing Behavior Research Articles

Intraspecific aggressiveness after lesions of midbrain raphe nuclei in rats.

Serotonin-depleting lesions of midbrain raphe (extensive lesions located within dorsal and partly median raphe muclei) induced intraspecific agressiveness in grouped Wistar male rats but failed to increase mouse-killing behaviour. Rats which had lesions in the lateral midbrain did not display intraspecific aggression nor mouse-killing activity. These animals showed unchanged levels of both serotonin and noradrenaline in the forebrain.

Biochemical correlates in mouse-killing behavior of the rat: brain acetylcholine and acetylcholinesterase after administration of Δ 9-tetrahydrocannabinol

Biochemical correlates in mouse-killing behavior of the rat: brain acetylcholine and acetylcholinesterase after administration of Δ 9-tetrahydrocannabinol

Changes in acetylcholine content in rat brain after bilateral olfactory bulbectomy in relation to mouse-killing behavior

Acetylcholine (Ach) content was measured in 5 discrete areas of rat brain following bilateral olfactory bulbectomy. The rats with olfactory bulbectomy (O.B. rat) exhibited significantly lower Ach levels in the cortex than intact and sham-operated controls. However, there was no significant difference in Ach level of all brain areas between the killer and non-killer O.B. rats. These results may suggest that cortical cholinergic function is activated by bulbectomy, but the change in cortical Ach level is not related to muricide.

Effect of a decarboxylase inhibitor (Ro 4-4602) on 5-HTP induced muricide blockade in rats

The effect of N'-( dl-seryl)-N 2(2,3,4-trihydroxybenzyl)-hydrazine (Ro 4-4602) on the blockade in the rat of muricidal behaviour caused by 5-hydroxytryptophan (5-HTP) was investigated. It had been previously reported that Ro 4-4602 exhibited dual actions on the antagonism by DOPA of reserpine effects on motor activity. This dual effect was also observed in the present study where 5-HTP and mouse killing behaviour are employed. Lower doses (2.5–10 mg kg ) of Ro 4-4602 enhanced while the dose of 25 mg kg of Ro 4-4602 decreased the blockade of the muricidal behaviour due to 5-HTP. The biochemical interaction of Ro 4-4602 and 5-HTP in the periphery and in the brain are speculated upon in an attempt to explain the data.

Effects of psychotropic drugs on hyperemotionality of rats with bilateral ablations of the olfactory bulbs and olfactory tubercles.

The effects of psychotropic drugs on hyperemotionality of the rat with lesions in the olfactory system, including the olfactory bulbs and olfactory tubercles (O.B.-O.T. rat), were investigated, and compared with the neurotoxic effects of these drugs measured on rotarod performance of the mice with bilateral olfactory bulb ablations (O.B. mice). Chlorpromazine, reserpine and meprobamate inhibited the hyperemotionality at doses close to their neurotoxic dose. Pentobarbital showed only a slight effect on the hyperemotionality at subhypnotic doses. Chlordiazepoxide, diazepam and haloperidol markedly inhibited the hyperemotionality at lower doses without causing neurotoxicity. Imipramine and arnitriptyline selectively inhibited mouse-killing behavior (muricide) of the O.B.-O.T. rat without affecting the other hyperemotional responses to various stimuli, thus differing from tranquilizers. The mode of action of these drugs in the O.B.-O.T. rat was essentially the same as observed in either the O.B. and the septal rats. For evaluating the effects of psychotropic drugs, the O.B.-O.T. rats are superior to the O.B. and septal rats, as they share both offensive aggression of the O.B. rat and hyperreactivity of the septal rat, and furthermore they exhibited muricide in a much higher incidence soon after the brain lesions.

Effects of psychotropic drugs on hyperemotionality of rats with bilateral ablations of the olfactory bulbs and olfactory tubercles

The effects of psychotropic drugs on hyperemotionality of the rat with lesions in the olfactory system, including the olfactory bulbs and olfactory tubercles (O.B.-O.T. rat), were investigated, and compared with the neurotoxic effects of these drugs measured on rotarod performance of the mice with bilateral olfactory bulb ablations (O.B. mice). Chlorpromazine, reserpine and meprobamate inhibited the hyperemotionality at doses close to their neurotoxic dose. Pentobarbital showed only a slight effect on the hyperemotionality at subhypnotic doses. Chlordiazepoxide, diazepam and haloperidol markedly inhibited the hyperemotionality at lower doses without causing neurotoxicity. Imipramine and amitriptyline selectively inhibited mouse-killing behavior (muricide) of the O.B.-O.T. rat without affecting the other hyperemotional responses to various stimuli, thus differing from tranquilizers. The mode of action of these drugs in the O.B.-O.T. rat was essentially the same as observed in either the O.B. and the septal rats. For evaluating the effects of psychotropic drugs, the O.B.-O.T. rats are superior to the O.B. and septal rats, as they share both offensive aggression of the O.B. rat and hyperreactivity of the septal rat, and furthermore they exhibited muricide in a much higher incidence soon after the brain lesions.

Effects of acute and chronic administration of [formula omitted] extract on the mouse-killing behavior of rats

The muricidal behavior of spontaneous killer rats was blocked after the first injections of an extract of Cannabis sativa corresponding to 8.8 mg of Δ9-tetrahydrocannabinol. On the contrary, to rats which did not show this behavior spontaneously, the chronic administration of the extract induced mouse-killing behavior; this effect of marihuana was potentiated by starvation which, by itself, did not interfere with the behavior of the non-killer rats. These results tend to support the view that cannabis has a dual action. Suppression of muricidal behavior may occur due to the acute depressant effects of marihuana. Under chronic administration, however, tolerance develops to these effects unmasking hyperemotionality and/or irritability which may induce killing behavior in previously non-killer rats.

Selective Blockade of Muricidal Activity in the Rat by Anorectic Agents

The ability of several anorectics to block selectively mouse killing in the rat was examined. A significant ratio between the muricide ED50 and the ED50 of a drug to produce debilitation in rotarod performance is a measure of selectivity. The mouse-killing behavior of a rat can be blocked with certain drugs at doses that do not render the animal debilitated. This selectivity, determined by the ratio of ED50′s, was found in the four anorectics examined as follows: diethylpropion dextroamphetamine aminorex fenfluramine.

Drug-induced conditioned aversion to mouse-killing in rats

Posttrial administration of atropine methylnitrate (MA) to rats that kill mice resulted in a marked inhibition of mouse-killing behavior. This conditioned aversion to mouse-killing after treatment with MA was more readily produced in rats fed ad lib than in those on a restricted food regimen. Food-deprived rats demonstrated a greater incidence of predatory behavior (i.e., consumption of the prey) than did killer rats not deprived of food. Predatory behavior appeared more sensitive to this conditioned aversion procedure than did the act of killing.

Effets de lésions du tegmentum ventral du mésencéphale sur le comportement d'agression Rat-Souris

Electrolytic lesions of the ventromedial region of the mesencephalic tegmentum (TVM) entail a transient abolition of the rat's mouse killing behavior, a transient anorexia or aphagia, and a transient depression of self-stimulation responses at lateral hypothalamic sites. These behavioral deficits may appear singly or in diverse groupings, and the differences from one animal to another cannot be explained on the ground of localization or extension of the individual lesions. Most animals recover the mouse killing behavior at a moment when they are still anorexic or aphagic and when the frequency of their self-stimulation responses is still below 10% of the stable preoperative level. The TVM takes part in mechanisms that facilitate the release of the mouse killing behavior; there exists in this respect a functional synergia between the TVM and the lateral hypothalamic area. Bilateral lesions of the ventral tegmental area of Tsai that interrupt fiber connections between the TVM and the lateral hypothalamus, do not even transiently modify the rat's mouse killing behavior.

Stimulation electrique du thalamus dorsomédian et comportement d'agression interspécifique du Rat

Stimulation of the dorsomedial thalamus does not elicit interspecific aggressive behavior in the rat. Whether epileptogenic or not, the thalamic stimulation regularly provokes an inhibition of the rat's mouse-killing behavior.

Mouse-killing behavior (muricide) induced by Δ9-tetrahydrocannabinol in the rat

Natural Δ 9-tetrahydrocannabinol (THC) was found to induce a characteristic mouse-killing behavior (muricide) in rats upon chronic administration. In the rat housed individually, this muricide developed even on the first day of administration, and continued for a long period of time even after withdrawal of the drug.

Contribution of midbrain structures to the control of the rat's mouse-killing behaviour: J. P. Chaurand, M. Vergnes, P. Schmitt and P. Karli — Laboratoire de Neurophysiologie, Centre de Neurochimie du CNRS, Strasbourg (France)

Contribution of midbrain structures to the control of the rat's mouse-killing behaviour: J. P. Chaurand, M. Vergnes, P. Schmitt and P. Karli — Laboratoire de Neurophysiologie, Centre de Neurochimie du CNRS, Strasbourg (France)

Evidence for inhibition by brain serotonin of mouse killing behaviour in rats.

THERE is some doubt about the role of brain serotonin in aggression. In mice made aggressive by prolonged isolation, there is a decrease in brain serotonin turnover1, while increased aggressiveness has been noted in cats2 and rats3 given p-chlorophenylalanine (PCPA), which inhibits serotonin synthesis4, although the experiments with cats2 were not confirmed later5. Dominguez and Longo6 reported that PCPA attenuates irritability and viciousness in rats with septal lesions, and Welch and Welch7 observed decreased aggressiveness in isolated mice given PCPA. The explanation for these contradictory results may be that different models of aggression are not mediated through the same areas of the brain or by the same biochemical mechanisms.

Comportement d'agression interspe´cifique et comportement alimentaire du rat: Effets de le´sions des noyaux ventro-me´dians de l'hypothalamus

Bilateral lesions of ventromedial hypothalamic nucleus induce emotional hyper-reactivity in most rats, but induce mouse-killing behaviour in only about 30% of operated animals. These lesions may also elicit hyperphagia, anodal lesions being more effective than cathodal ones. Of the 29 rats that have shown behavioural changes entailed by the ventromedial hypothalamic lesion, only 5 have shown both clear hyperphagia and interspecific aggressive behaviour, the 24 others showing one or the other of these behavioural changes.

Quipazine, a new type of antidepressant agent.

Quipazine, (2-(1-piperazinyl)quinoline), is comparable to the tricyclic antidepressants in many of its pharmacological effects. Common properties include the ability to antagonize reserpine and tetrabenazine sedation in mice and rats, to reverse reserpine hypothermia in rats and to inhibit selectively the mouse-killing behavior of rats. In all these actions, quipazine is approximately equipotent with imipramine, desipramine and amitriptyline. Quipazine is far less effective than imipramine in potentiating the locomotor stimulation elicited by d-amphetamine. Quipazine differs from tricyclic antidepressants in that it does not enhance responses induced by exogenous or endogenous norepinephrine and does not block the effects of indirectly acting sympathomimetic amines. Furthermore, quipazine, unlike imipramine, counteracts tetrabenazine induced sedation in catecholamine depleted animals. These findings suggest that the pharmacological actions of quipazine do not involve adrenergic mechanisms.

Déclenchement d'un comportement d'agression par stimulation électrique de l'hypothalamus médian chez le rat

Interspecific aggressive behavior was elicited in natural non-killers by electrical stimulation of various sites located in the ventro-medial and dorso-medial hypothalamus. Intense emotional reactions and flight responses were regularly associated with the experimentally induced mouse-killing behavior. Emotional reactions and flight responses without any aggressive behavior were elicited from other sites located within the same hypothalamic region.

Neurochemical effects of imipramine and amphetamine in aggressive mouse-killing (muricidal) rats

Mouse killing (muricidal) rats have been shown to have higher forebrain levels of norepinephrine than control non-killer rats. In addition, they elicit higher rate constants for the decline of 3H-norepinephrine given intraventricularly into the brain and, consequently, much higher turnover rates for norepinephrine than controls (non-killers). These differences have not been obtained in the hindbrain region. No differences in the levels or rate of turnover of serotonin have been observed in either brain region studied. Furthermore, the elevated rate constant seen in forebrain norepinephrine turnover studies using the isotopic procedure has not been observed in non-isotopic turnover studies in which α-methyl- p-tyrosine was used to inhibit tyrosine hydroxylase. Differences between the two methods may be attributable to the inhibitory action of muricidal behavior by α-methyl- p-tyrosine. The effects of imipramine and amphetamine on norepinephrine turnover in the forebrain of killer rats have been compared with those of drug-treated, non-killer rats as well as with untreated rats. Both agents, given at doses which inhibit mouse-killing behavior, accelerate the turnover rate of brain norepinephrine in non-killer rats; however, they do not influence the previously elevated levels of norepinephrine nor the elevated rate constants and turnover rate for this amine in killer rats. Suggestions involving altered reuptake mechanisms, as well as divergent effects of the antidepressants in muricidal rats, have been offered to explain these differences.

Structural relationship and potency of agents which selectively block mouse killing (muricide) behavior in rats

Rat muricidal activity has been shown to be selectively inhibited by some antidepressants, antihistaminics and stimulants. Several agents from each class, including representative structural prototypes, were tested for anti-muricidal activity. Selective inhibition was considered only when it occurred at doses which were significantly lower than those impairing rotarod performance. The order of potency for agents found selectively active in this study was: tranylcypromine > methamphetamine > d-amphetamine > desipramine > imipramine > chlorpheniramine > pargyline. Structurally each of these drugs has a sidechain substitution which is an alkylamine. However, not all drugs with alkylamine sidechains were selectively effective. These studies seem to indicate those agents structurally related to d-amphetamine, i.e., methamphetamine and tranylcypromine, are the most potent selective inhibitors of mouse killing behavior in rats.