Mouse-killing In Rats Research Articles

Comparative study of the effect of 3-carboxy-?-carboline methylamide and diazepam on rat behavior

The effects of benzodiazepine receptor agonist, diazepam, and inverse agonist, FG 7142, were examined. Strong antagonism between FG 7142 (10 mg/kg) and diazepam (1 mg/kg) activity was revealed in the open field test. On the other hand, both FG 7142 and diazepam inhibited isolation-induced intraspecies aggressive behaviour of rats. FG 7142 also reduced interspecies aggression of mouse-killing rats. The findings suggest that both diazepam and FG 7142 have antiaggressive properties in the isolation-induced aggression model, which are mediated by benzodiazepine receptors of the central nervous system.

Spontaneous mouse killing rats: Gentling and food deprivation result in killing behavior almost identical to that of rats with medial hypothalamic lesions

Rats that were found to kill a mouse spontaneously were divided into two groups. One group was left untreated and allowed free access to food while the other was gentled for 15 min/day and given only 15 g of food/day. Nonkilling rats were induced to kill mice by lesions of the medial hypothalamus. Seven to ten days after being divided into groups or subjected to brain lesions, each rat's behavior toward a series of stimuli was observed. The stimuli were a live mouse, a second live mouse, a freshly killed mouse, and a cotton wad. Food-deprived/gentled spontaneous killers and rats induced to kill by medial hypothalamic lesions each tended to attack with higher intensities and lower latencies than control spontaneous killers. The food-deprived/gentled spontaneous killers and lesion-induced killers (but not the control spontaneous killers) also attacked a dead prey moved vertically and then held onto the prey with sufficient intensity that their feet would leave the floor of the cage before they would release their grip on the prey. It is argued that the behavior of food-deprived spontaneous killers may constitute a more valid model of spontaneous mouse killing than that of sated spontaneous killers. The close correspondence between behavior toward a prey by lesion-induced killers and food-deprived spontaneous killers suggests that the lesion-induced killers fit this model of mouse killing remarkably well.

Medial hypothalamic and medial accumbens lesions which induce mouse killing enhance biting and attacks on inanimate objects

The response to a series of objects by rats with lesions of the medial hypothalamus or medial accumbens was compared to that of spontaneous killing rats and sham-lesioned nonkillers. When exposed sequentially to a piece of wood, a wad of cotton, or a freshly killed mouse, there were no differences in the intensity of the initial response toward the stimulus object by spontaneous mouse killing rats and lesioned animals that were later shown to kill mice. However, lesioned animals did spend more time biting these objects and were more likely than spontaneous killers to attack the objects if they were moved about by the experimenter. When allowed to kill mice, there were no differences in the intensity of the attack by spontaneous and lesion-induced killers but again the lesioned animals bit the prey more following the kill and were more likely to attack the dead prey when it was moved by the experimenter. Sham-lesioned nonkillers spent less time biting the stimulus objects than spontaneous killers and never attacked the objects when they were moved by the experimenter. It is argued that the killing of lesioned animals is homologous to that of spontaneous killers but that the lesioned animals exhibit most components of the predatory behavior to an exaggerated degree.

Individual differences in interspecific aggressiveness: Mouse-killing in rats after isolation

Measures of extraversion and neuroticism in rats are related to aggressive behaviour in two strains of rats. Isolated rats and rats reared together, of the Sprague-Dawley and Wistar strains, were submitted to an aggressiveness test. The results show that isolation generates and/or increases mouse-killing behaviour only in Wistar rats which are more emotional (neurotic) than Sprague-Dawley rats. The two strains do not differ significantly in their open-field ambulation (extraversion), although Wistar rats tend to be less ambulatory. Within the Wistar strain, the results showed the same trend, that is, the more emotional and less ambulatory rats (dysthymics) are the ones who became killers after isolation. The Sprague-Dawley strain does not show any significant aggressive behaviour after isolation.

A comparison of prey eating by spontaneous mouse killing rats and rats with lateral septal, medial accumbens, or medial hypothalamic lesions

Rats with lesions of the medial hypothalamus and spontaneous mouse killing rats were tested for mouse and rat pup killing in their living cages 1 and 3 days postoperatively. The lesioned and spontaneous killers did not differ significantly in amount of prey eaten within 10 min following a mouse kill on either Day 1 or 3 postoperatively. Both groups ate significantly more of the prey than did sham-lesioned rats that were presented with a freshly killed mouse. When 4 hr was allowed for eating following a kill, rats with lesions of the lateral septum, medial accumbens, and medial hypothalamus each ate significantly more than spontaneous mouse killing rats. The greater prey eating by the lesioned animals is probably not the result of the prey being a highly palatable food since rats with medial hypothalamic lesions but not those with medial accumbens or septal lesions showed enhanced consumption of a sweetened lab chow over a 4 hr period. The quantitative similarity in the prey eating by spontaneous and lesion-induced mouse killers in the period immediately following the kill serves to further establish a relationship between these two kinds of killing. The greater eating that occurs in lesioned animals when a longer time is allowed for eating is consistent with other observations of excesses in the killing behavior of lesioned animals relative to spontaneous killers.

Dissociation of prey killing and prey eating by naloxone in the rat

Mouse killing rats matched for killing latency and prey eating were injected (IP) with 0.5, 2.0, or 5.0 mg/kg naloxone or 0.9% saline. Naloxone did not significantly inhibit prey killing or alter prey killing latency at any dose but did reduce prey eating by 50% at the two higher doses. The dissociation of prey killing and prey eating by naloxone is consistent with other evidence that these two behaviors are separate components of predation in rats.

Mouse killing in rats induced by lesions of the medial hypothalamus or medial accumbens: Short-term preoperative exposure to a mouse does not suppress the killing

Rats were either exposed or not exposed to a mouse in their living cage for a 48-hr period. At the end of this time a bilateral lesion was made in the medial accumbens region or in the medial hypothalamus. When tested 2 days postoperatively, the killing frequency among rats that had been exposed to mice preoperatively was not significantly lower than that of rats that were not preoperatively exposed. The ineffectiveness of preoperative experience in suppressing the mouse killing induced by medial accumbens and medial hypothalamic lesions is similar to that found previously with dorsal-median raphe lesions and olfactory bulb lesions and is in contrast to the ease with which preoperative experience prevents mouse killing induced by septal lesions and serotonergic lesions induced by 5,7-dihydroxytryptamine.

Induction of mouse-killing in the rat by intraventricular injection of a GABA-Agonist

Intracerebroventricular injections of THIP (2.5 and 5.0 μg in 5 μl) facilitated elicitation of mouse-killing in killer rats placed in a non-familiar environment. The same doses induced well organized mouse-killing responses in 60% of non-killer rats. Concomitantly food intake was elicited. Exploratory activity as well as orientation and approach towards any sensory stimulus were also increased. On the contrary, intracerebroventricular injections of bicuculline methiodide (65 and 125 ng in 5 μl) suppressed aggressive responses in killer rats. The data support the view that GABA receptors are involved in mechanisms which facilitate elicitation of mouse-killing behaviour as well as other positively motivated responses.

Mouse killing in rats: A comparison of spontaneous killers and rats with lesions of the medial hypothalamus or the medial accumbens nucleus

Mouse killing was observed and videotaped at forty-eight hr following surgery in rats with lesions of the medial hypothalamus or the medial accumbens. The initial attacks and killing bites of the lesioned rats were directed at the anterior dorsal surface, predominantly to the regions of the neck, shoulders, and thorax and did not differ from those of spontaneous mouse killing rats. The latency to attack was significantly shorter for the lesioned animals but the time required to kill following the attack tended to be longer. Lesioned animals spent significantly more time biting the prey following the kill and left significantly more bite marks on the prey than did the spontaneous killers. When the dead prey was moved about the cage following the kill, the lesioned animals showed a significantly greater tendency to attack it than did the spontaneous killers. Following the test of mouse killing, each rat was successively exposed to a freshly killed mouse, a cotton wad, and a wood block. The lesioned animals attacked the dead mouse and the cotton wad as though they were live mice whereas the spontaneous killers did not. These results suggest that while the killing is similar for lesioned and spontaneous killers, the lesioned animals show a heightened response to the killing experience. This is manifested in an exaggeration of attack behaviors toward prey and prey-like stimulus objects following an initial killing experience.

Effect of hypothalamic injections of 5,7-dihydroxytryptamine on elicitation of mouse-killing in rats

An overall and marked serotonin (5-HT) depletion of the brain was found to facilitate initiation of mouse-killing behavior in the rat, whereas more selective 5-HT depletions within forebrain structures such as the septum, hippocampus, cingular cortex and amygdala, did not have such an effect. In order to further investigate the topography of the 5-HT pathways and terminals thought to be involved in an inhibitory control over this behavior, localized lesions of the serotonergic system(s) were performed by means of bilateral 5,7-dihydroxytryptamine (5,7-DHT) injections (5 μg/μl) into the hypothalamus in naive rats. 5,7-DHT injections into the medial hypothalamus did not affect the initiation of mouse-killing behavior, whereas the reflexive startle responses to air puffs were increased. The animals' open-field behavior remained unchanged. Forebrain 5-HT content was reduced by 50% in this group. 5,7-DHT injections into the lateral hypothalamus increased the proportion of killers to 46% as compared to 10% in the control group, in spite of a reduced activity in the open-field and unchanged startle responses. Forebrain 5-HT content was reduced by 88%. As the lateral hypothalamus contains afferents from both the dorsal and the median raphe nuclei, it is likely that 5-HT terminals modulate some hypothalamic mechanism involved in the control of mouse-killing behavior.

Medial hypothalamic lesions in the rat enhance reactivity and mouse killing but not social aggression

In rats subjected to lesions of the medial hypothalamus, 8 of 11 animals became mouse killers and all manifested some degree of hyperreactivity to the experimenter. When introduced as intruders into a mixed sex colony group, the lesioned rats did not manifest piloerection nor did they emit flank attacks characteristic of social aggressive behavior. However, the lesioned animals did respond to the attacks of the resident male rats with significantly more counterattacks and biting than did sham-lesioned control rats. Spontaneous mouse killing rats also failed to show a level of social aggressive behavior significantly greater than that of sham-operated control rats, but the spontaneous mouse killers did kill rat pups in the colony groups. Alpha-male rats when introduced as an intruder into a colony group did exhibit piloerection and emit flank attacks characteristic of social aggressive behavior. These results demonstrate that the mouse killing and heightened reactivity associated with medial hypothalamic lesions do not represent an indiscriminant release of all forms of agonistic behavior.

Lesions of the region ventral to the anterior septum increase mouse killing and reactivity but not social attack

Rats with lesions in the region ventral to the anterior septum were tested in a novel situation for attack on a young adult rat and attack on a mouse. To determine whether they would also show enhanced social attack behavior, the lesioned animals that attacked the rat or killed a mouse in the paired encounter were tested 2 days later in a group colony composed of male and female adult rats and in some cases rat pups. Lesioned rats that attacked a young rat or killed a mouse in the paired encounter never developed piloerection or attacked resident males of the colony group. The lesioned animals did attack rat pups in the colony situation and also attacked females in the vicinity of the rat pups. Spontaneous mouse-killing rats also failed to attack males in the colony groups, but did attack rat pups and females. Alpha-male rats did develop piloerection and attacked resident males when introduced as intruders into a colony group. The alpha males did not attack rat pups or females in the colony group. Two of nine sham-operated rats developed piloerection and attacked males in the colony group situation, although none attacked the rat pup or the mouse in the paired encounter. It is inferred that rats with lesions ventral to the anterior septum do not show enhanced intraspecific social attack behavior similar to that of alpha-male rats.

Mouse and weanling rat killing by spontaneous mouse killing rats, and by rats with lesions of the lateral septum or the region ventral to the anterior septum: Similarities in killing latency and prey eating

Mouse and rat pup killing by male rats with lesions of the lateral septum or of the region ventral to the anterior septum were compared with that of spontaneous mouse killing rats. Latency to kill, latency to eat, and the amount of the prey eaten were similar for all groups. The killing and eating of weanling rats and mice were also similar across groups and occurred in a novel environment as well as in the home cage. However, the tendency to kill weanling rats is significantly higher in lesioned animals that kill mice than in natural killers which kill mice. In addition, some lesioned rats but no unlesioned rats also killed and ate young (150 to 200 g) male rats. It is argued that the killing behavior of rats with lesions of the lateral septum or of the region ventral to the anterior septum represents an enhanced predatory behavior.

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

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

5,7-dihydroxytryptamine-induced mouse killing and behavioral reversal with ventricular administration of serotonin in rats

In order to establish a more complete behavioral profile on animals induced to kill mice following serotonin depletion, naturally non-mouse-killing male Long-Evans rats were administered 5,7-dihydroxytryptamine (5,7-DHT) in a saline-ascorbic acid vehicle or vehicle alone to the left lateral ventricle through a chronically indwelling cannula. Following a postsurgical delay, animals were tested for mouse killing, food and water consumption, spontaneous motor activity, and exploratory behavior. 5,7-DHT treatment resulted in a significant increase in the incidence of mouse killing over vehicle-injected controls in the absence of effects on the other behaviors investigated. In a second experiment, 5,7-DHT-treated rats from Experiment I were administered small doses of serotonin intraventricularly. An additional group of spontaneously mouse-killing rats also received intraventricular injections of serotonin. This manipulation led to a significant increase in the latency of both groups to kill mice over both preinjection latencies and vehicle-injected control animals. Since serotonin depletion resulted in the induction of mouse killing in naturally nonkilling rats without affecting other potentially contributory behaviors and since the mouse killing could be reversed by intraventricular administration of serotonin an inhibitory role for serotonin in the mediation of mouse killing is suggested.

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.

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.

The interaction of hunger, feeding, and experience in alteration of topography of the rat's predatory response to mice

Hooded rats which begin to kill mice while deprived of food display an orderly development of attack topography. Attack complexity is maximal at onset of killing when four component attacks comprising chasing, carrying, pawing, and biting mice predominate. Attack simplifies to two component pawing-biting attacks with repeated killing experience which result in rapid kills. Food satiation and a gradual decline in killing behavior reinstates attacks of intermediate complexity, comprised of chasing, pawing and biting. Redepriving the rats of food immediately results in simple and rapidly lethal pawing-biting attacks. With further killing experience some rats show the chasing-pawing-biting attacks once again. The data suggest that prey self-defense and the sensitivity of attacking rats to prey defense account for variation in some aspects of attack complexity. Factors intrinsic to the rat and dependent upon response to food deprivation and experience of killing account for other aspects of attack topography. Rats which do not begin to kill mice while food deprived show simple and fragmented attack topography unlike that of mouse-killing rats. The study was written for publication while the first author was supported by a grant to Drs. Goddard and Adamec from NIMH, grant number MH25995-02, and by Dr. Kenneth Livingston and the Scott Laboratory. The critical reading of the manuscript by Alex Stiglick is also gratefully acknowledge.

The effects of food deprivation and the length of the test on muricide in rats

Long-Evans hooded rats were divided into three feeding conditions: ad lib, deprivation, or deprivation/ad lib. Approximately one-half of the animals received a 5-min mouse-killing test while the remaining animals received a 20-min, 24-hr mouse-killing test. Results indicate that food deprivation is a powerful determinant of the initiation of mouse killing in rats, but subsequent maintenance of the killing response is less dependent of feeding schedules. The probability of mouse killing is not affected by shifting deprived rats to an ad lib feeding schedule; however, response latencies are significantly increased by this manipulation. In addition, the results of this study indicate the need for future research to determine a standard and optimum mouse-killing test duration.

Morphine action in grouped and isolated rats and mice.

The present study determines the analgesic effects of morphine in grouped and isolated rats and mice. Isolated animals developed altered behavioral patterns, including mouse-killing in rats and mutual aggressiveness in mice. The analgesic effect of morphine was tested by tail compression in rats and by the hot plate for mice. Isolated rats developing mouse-killing behavior had a raised pain threshold, while indifferent animals (nonkillers) responded less to morphine. Isolated mice, particularly low aggressors, gave enhanced responses to morphine.