Mouse-killing Behavior Research Articles

Mouse-killing and hyperemotionality in rats induced by three different kinds of experimental manipulations: A comparative study

Male rats were subjected to one of three different kinds of manipulations: isolation housing, bilateral olfactory bulbectomy, and Δ9-tetrahydrocannabinol (THC) administration. All three treatments produced an increase in the tendency toward mouse-killing behavior and also affected the animal’s emotionality. Each of these treatments, however, produced distinctive features in both the topography of killing response and hyperemotionality. Among the three models, isolation-induced killer rats exhibited the most well-organized killing response, while in both olfactory bulbectomy and THC-induced killer rats the killing response was characterized by inefficient, compulsive, and indiscriminate biting. The satiation of mouse-killing behavior did not occur in any of the three models. Isolation-induced killer rats were more reactive in startle response than were nonkiller rats, while THC-induced killer rats showed a higher reactivity to the presented wooden rod than did nonkiller rats. In olfactory bulbectomized rats, there was no significant difference in any behavioral items between killer and nonkiller rats. This evidence suggests that the mouse-killing behavior in rats is not a unitary phenomenon and that various physiological and psychological bases exist, depending upon the manipulation employed.

Regional changes in brain norepinephrine content in relation to mouse-killing behavior by rats

Three separate series of experiments were conducted as follows: isolation housing, bilateral olfactory bulbectomy, and Δ 9-tetrahydrocannabinol (THC) administration. All three experimental manipulations produced an increase in the incidence of mouse-killing behavior. In order to elucidate the possible neural mechanisms mediating the killing response, norepinephrine (NE) content was measured in 6 discrete areas of the brain (the cortex, striatum, amygdala, midbrain, hypothalamus, and pons plus medulla oblongata). Following isolation housing, no significant difference in NE levels of any of the brain areas was demonstrated between the aggregated and isolated rats, nor between the killer and nonkiller rats. The rats with olfactory bulbectomy exhibited high NE content in the hypothalamus as compared with the intact or sham-operated rats, but there was no significant difference between the killer and nonkiller rats. After injection of THC, NE content in both the hypothalamus and pons plus medulla oblongata was decreased independent of the manifestation of killing response. The evidence indicates no regional change in brain NE levels specific to the killing response and suggests that brain NE may not participate in the mediation of mouse-killing behavior.

L-tryptophan's effects on mouse killing, feeding, drinking, locomotion, and brain serotonin

Injections of the serotonin precursor l-tryptophan (25, 50, and 100 mg/kg IP), inhibited mouse killing behavior in rats, as indicated by a dose dependent increase in latencies to attack and kill mice. Tests in 24 hr food deprived rats revealed that feeding behavior was also significantly decreased by about 30% by tryptophan injections (50–100 mg/kg IP). Concomitant with the behavioral changes were increased levels of brain serotonin and its metabolite 5-hydroxyindoleacetic acid. Drinking, latencies to sniff mice, and ability to locomote on a rotating rod were not affected by l-tryptophan injections, although spontaneous activity in an open field was reliably reduced by 33% with a dose of 100 mg/kg. thus, while the degree of selectivity for tryptophan's effects on behavior remains open to question, these findings are consistent with hypotheses of an inhibitory role for central serotonergic systems, particularly in mouse killing and feeding behaviors.

Effects of Stimulation of the Raphe Nuclei on Muricide Behavior in Rats

Mouse-killing behavior was induced in male Wistar rats by chronic isolation. Selective stimulation of the dorsal raphe nucleus markedly reduced this aggressive behavior. On the other hand, stimulation of the median raphe nucleus produced no changes in muricide behavior. Our results indicate that dorsal and median raphe nuclei function differentially in the regulation of muricide behavior with the dorsal raphe playing a critical role in this behavioral pattern.

Effects of electroconvulsive shock on mouse-killing behavior (muricide) in olfactory bulbectomized rats.

We investigated the influence of electroconvulsive shock (ECS), regarded to possess an antidepressant effect clinically, on muricide in olfactory bulbectomized rats (OB rats). Muricide in these rats was markedly inhibited by ECS treatment. Five and 10 min after the termination of ECS-induced convulsions, muricide was inhibited by 100%. Even after intervals of 20 and 60 min, inhibition rates of 80% and 30% were obtained, respectively. ECS-induced muricide inhibition was remarkably antagonized by pretreatment with the alpha-blocker phenoxybenzamine but not by pretreatment with the beta-blocker sotalol. ECS-induced suppression of muricide was potentiated by repeated ECS treatment once daily for 10 days. After several applications of ECS treatment, muricide was inhibited in muricide tests done 24 hours after ECS treatment; this state persisted for up to 10 days thereafter. The results of this experiment demonstrated that ECS treatment specifically inhibited muricide in OB rats and further suggested that the cerebral noradrenergic alpha-receptor system plays an important role in this ECS-induced inhibition of muricide. Similar findings in the case of antidepressant administration, inhibition of muricide was potentiated by chronic ECS treatment. Specific inhibition of muricide in OB rats by antidepressants indicated that this phenomenon may serve as an animal model for the evaluation of antidepressant activity. Our results reiterate the usefulness of muricide in OB rats as an excellent experimental model for the assessment of antidepressant activity.

Effect of stimulation of brain serotonergic system on mouse-killing behavior in rats

Mouse-killing behavior was induced in male Wistar rats due to 6 weeks isolation. The selective stimulation of the dorsal raphe nucleus markedly reduced muricide behavior. On the other hand rats with electrodes situated outside of the dorsal raphe (within the substantia grisea centralis) showed no changes in muricide behavior when compared with control (non-stimulated) animals. Pharmacological stimulation of whole serotonergic brain neurons by quipazine, an agonist of serotonin receptors, and compound CGP 6085-A, a selective inhibitor of serotonin uptake, strongly decreased mouse-killing behavior. Our data indicates that serotonergic neurons inhibit predatory aggression in rats.

Variability in rat irritable and predatory aggression

Rats from differing strains and/or suppliers show marked differences in the stability and frequency of shock-induced fighting under uniform parameters. Similar differences occur in mouse-killing behavior. Aggression differences are not necessarily related to differences in footshock sensitivity. Such behavioral variability can be used to correlate strain-dependent neurochemical and behavioral characteristics.

Mouse-killing in rat induces a naloxone-blockable increase in nociceptive threshold

Mouse-killing behaviour in rats increased the nociceptive threshold for paw licking, as measured in the hot-plate test. This effect was prevented by the opiate antagonist naloxone, which, on the other hand, had no influence on mouse-killing behavior per se. It is concluded that opioid mechansims may be involved in changes of nociceptive threshold associated with aggressive behavior.

Effects of lesions of the ventral noradrenergic bundle on aggressive behavior in rats

Bilateral lesions in the ventral noradrenergic bundle decreased shock-induced fighting behavior in rats. On the other hand, these lesions failed either to change mouse-killing behavior in isolated rats or to induce this behavioral pattern in natural non-killers.

Predatory behavior after hypothalamic lesions in cats

Electrolytic lesions of the hypothalamus were performed in cats tested preoperatively as good mouse killers. It was found that mouse killing behavior was not impaired after hypothalamic damage, whereas mouse consumption was abolished for several weeks. Food intake was transiently diminished in most cats, but after a few days it reached or surpassed the preoperative level. It was concluded that ventro-postero-lateral hypothalamic lesions impair specific motivation for eating the prey.

Synergy or potentiation of sodium valproate and an inhibitor of GABA uptake

(R,S)-nipecotic acid, which inhibits GABA uptake in vitro, has only a slight effect on mouse-killing behaviour. (R,S)-nipecotamide maleate (NCS-3), injected IP (50–150 mg/kg) or per os (0.5-1.5 g/kg) to muricidal rats produces an inhibition of this agressive behaviour. Coadministration of suboptimal doses of NCS-3 and the GABA-inhibitor sodium valproate produce a marked potentiation when given by the intraperitoneal route and a striking synergistic effect when given orally. This results provide supplementary evidence that the inhibition of killing behaviour by these drugs is due to a potentiation of a central GABA-ergic system.

A comparison of the effects of acute and subacute administration of β-phenylethylamine and d-amphetamine on mouse killing behavior of rats

β-Phenylethylamine (PEA) is an endogenous amine that in some instances acts biochemically and behaviorally like amphetamine. In the present experiments, the effects of PEA on mouse killing by rats were compared and contrasted with the effects of d-amphetamine on this behavior. When given acutely to experienced mouse killing rats, PEA (16 and 32 mg/kg) inhibited killing in a direct dose dependent manner. This is similar to the dose dependent inhibition of killing by amphetamine reported previously. However, d-amphetamine but not PEA showed physiologic tolerance following 8 days of twice daily administration. Cross tolerance between the two drugs only occurred when d-amphetamine was administered subacutely. It was concluded that PEA and d-amphetamine have similar acute effects but differed when given subacutely since PEA did not show tolerance and there was not bidirectional cross-tolerance. These data suggest that these drugs have different pharmacologic actions when given repeatedly. One possible difference may be the duration of action.

Manipulations of dietary tryptophan: Effects on mouse killing and brain serotonin in the rat

Maintaining rats on a tryptophan-free diet for 4–6 days induced mouse killing in non-killer rats, and significantly facilitated killing in killer rats, as indicated by shorter latencies to kill the mice. The killing responses were similar in topography to the natural killing responses. These changes in killing behavior did not appear to be due to generalized changes in irritability. The increased killing after maintenance on a tryptophan-free diet was accompanied by a 26% reduction in brain serotonin (5-HT) and a 29% reduction in brain 5-hydroxyindoleacetic acid (5-HIAA). When the tryptophan-free diet was supplemented with l-tryptophan (0.5 or 2%), brain 5-HT and 5-HIAA were increased above control levels, and the rat's killing response appeared normal both in terms of latency and topography, similar to that seen in control chow fed animals. While rats consumed less of the tryptophan-free and tryptophan supplemented diets, control subjects deprived of chow such that they lost as much weight as rats fed the tryptophan-free diet, did not show changes in killing behavior. These results are consistent with the hypothesis that central serotonergic systems exert inhibitory control over mouse killing behavior in rats.

Effects of long-term isolation on aggressive behavior and excitability of the rat with olfactory bulbectomy

Differential effects of aggregated housing and isolated housing were investigated on the occurence of hyperemotionality and mouse-killing behavior (muricide) in the rat with olfactory bulbectomy (O.B. rat). The emotional responses to stimuli of the O.B. rat were markedly increased in score in aggregated housing as well as in isolated housing within a week after surgery. After 80 days, however, the O.B. rats in isolated housing exerted significantly higher hyperemotionality than those in aggregated housing. The occurrence of muricide was approximately 30% in the isolated O.B. rats and 20% in the aggregated O.B. rats at 2 weeks after surgery, thereafter that in the former further increased to 50% on the 46th day and finally to 100% on the 150th day, while that in the latter remained unchanged throughout the experimental period of 150 days.

Effects of early amygdaloid lesions on the development of reactivity in the rat

When carried out in 7–8 day old rats housed in grouped condition following weaning, bilateral amygdaloid lesions provoke a lasting hyperreactivity in terms of increased locomotor activity and higher rearing scores in the openfield. The lesion-induced hyperreactivity which is clearly apparent at 40 days and which persists till adult age, is less marked if the weaned rats are housed in isolation. When carried out at the age of 25 days, amygdaloid lesions enhance even more the rat's responsiveness to a novel environment. Early amygdaloid lesions provoke a marked increase in the proportion of rats that display mouse-killing behavior when adult, a behavioral effect that can be linked up with their hyperreactivity. On the contrary, bilateral amygdaloid lesions carried out in adult rats (at 3 months of age) do not change their responsiveness in the open-field, and only a small proportion of the lesioned rats (35 percent) spontaneously display mouse-killing behavior. It is concluded from the data obtained that the amygdala is involved in two closely related processes which play an important role in the ontogenetic development of the rat's reactivity and social responses. On the one hand, the amygdala takes an essential part in the setting up of a stable inhibition of aggressive responses on the basis of social interactions; on the other hand, it is involved in mechanisms which progressively lessen in a more general way the organism's reactivity to its environment.

The role of electrically excitable mesencephalic behavioral mechanisms in naturally occurring attack and ingestive behavior

Electrical stimulation of the mesencephalon dorsolateral to the central gray has been shown to elicit mouse killing but not ingestive behavior. In contrast, stimulation of the ventrolateral portions of the mesencephalon elicits ingestive but not mouse killing behavior. The present experiment investigated the effects of radiofrequency lesions of these areas on naturally occurring muricide and eating. The results indicate that the areas originally outlined with electrical stimulation play a role in the naturally occurring forms of these behaviors and that at the level of the mesencephalon these mechanisms are anatomically partially segregated.

Relationship between .DELTA.9-tetrahydrocannabinol-induced mouse killing behavior on the rat and the metabolism of monoamines in the brain, particularly the olfactory bulb.

Abstract Δ9-Tetrahydrocannabinol (THC) induces a characteristic mouse-killing behavior (muricide) in rats (1). The neural mechanism underlying this abnormal behavior is not clearly understood, although some workers have shown that the metabolism of noradrenaline (NA) or serotonin (5HT) in rat brain is influenced by a single administration of THC (2, 3). Bilateral ablations of the olfactory bulb (OB) of the rat were shown to induce muricide (4), suggesting that the OB plays an important role in the manifestation of muricide. Effects of THC on the metabolism of monoamines in the OB have apparently not been reported, although there are numerous papers on THC and the metabolism of monoamines in the whole brain.

Relationship Between Δ9-Tetrahydrocannabinol-Induced Mouse Killing Behavior on the Rat and the Metabolism of Monoamines in the Brain, Particularly the Olfactory Bulb

Δ9-Tetrahydrocannabinol (THC) induces a characteristic mouse-killing behavior (muricide) in rats (1). The neural mechanism underlying this abnormal behavior is not clearly understood, although some workers have shown that the metabolism of noradrenaline (NA) or serotonin (5HT) in rat brain is influenced by a single administration of THC (2, 3). Bilateral ablations of the olfactory bulb (OB) of the rat were shown to induce muricide (4), suggesting that the OB plays an important role in the manifestation of muricide. Effects of THC on the metabolism of monoamines in the OB have apparently not been reported, although there are numerous papers on THC and the metabolism of monoamines in the whole brain.

Effects of psychotropic drugs injected into the limbic structures on mouse-killing behavior in the rat with olfactory bulb ablations

Effects of psychotropic drugs injected into the limbic structures on mouse-killing behavior in the rat with olfactory bulb ablations

A research on the action of testosterone propionate and of ciproterone acetate on the mouse-killing behaviour of the adult rat.

Data demonstrate exactly that testosterone favour above all the killing behaviour of castrate males at birth in comparison with control males while ciproterone acetate turns out to be more effective in diminishing the killing behaviour of males having integral testicle and of androgenized females at birth in comparison with castrated males. The results point out that the killing behaviour of rats is affected by the presence of testosterone in the first days of life, and in the grown-up animal.